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PHYS 203 Class 1 Nervous System – master controlling and communicating system of the body 3 major functions sensory function integration motor function Nervous system is divided into 2 parts Central nervous system brain and spinal cord integrating and command centre Peripheral nervous system nerves outside the CNS that extend from the brain and spinal cord communication lines linking the body to the CNS Peripheral NS is further divided functionally Sensory / Afferent Division “carry towards” nerve fibers that carry info from sensory receptors to the CNS somatic afferent fibers and visceral afferent fibers Motor / Efferent Division “carry away” nerve fibers that carry info from CNS to effector organs - muscles and glands Motor / Efferent Division has 2 parts Somatic Nervous System Voluntary Nervous System Autonomic Nervous System Visceral motor nerve fibers Involuntary Nervous System Cells of the Nervous System Astrocytes (CNS) make exchanges between capillaries and neurons control chemical environment around neurons Microglia (CNS) monitor health of neurons –phagocytize invading microorganisms or injured/dead neuronal debris Ependymal Cells (CNS) line central cavities of brain and spinal cord form a permeable barrier between the CSF and the tissue fluid in the CNS Oligodendrocytes (CNS) wrap their processes around the neurons producing myelin sheath Satellite Cells (PNS) surround neuron cell bodies Schwann Cells (aka neurolemmocytes) (PNS) form myelin sheaths Neurons conduct messages in the form of nerve impulses from one part of the body to another extreme longevity amitotic high metabolic rate Cell Body the major biosynthetic centre of the neuron clusters of bodies in CNS = nuclei clusters of bodies in PNS = ganglia Processes bundles of processes in CNS = tracts bundles of processes in PNS = nerves Dendrites the receptive/input region send incoming messages toward cell body the signals are graded potentials not action potentials Axon conducting region of the neuron generates and transmits nerve impulses away from cell body axolemma = axon cell membrane axon hillock = cone shaped area of cell body where axon arises from nerve fiber = long axon axon collaterals = branches terminus = axon end terminal branches, telodendria = branches at end axon terminals, synaptic knobs, synaptic boutons = knob-like endings at ends of terminal branches, the secretory region for neurotransmitters Transmission Path impulse generated at jctn of hillock and axon (called trigger zone) impulse along axon to axon terminals impulse arrives at end of terminal impulse causes stored signaling chemicals – neurotransmitters – to be released into ECF space NT excites or inhibits other neurons or effector cells Myelin Sheath and Neurilemma protects and insulates fibers increases nerve impulse transmission speed myelinated fibers – rapid nerve impulses unmyelinated fibres – slow nerve impulse PNS schwann cells form the myelin sheath by forming concentric layers. neurilemma – outer portion of schwann cell outside myelin sheath nodes of Ranvier / neurofibril nodes – gaps between adjacent schwann cells, axon collaterals emerge here unmyelinated fibers – schwann cells form up to 15 or more recessed areas for axons, usually thin axons CNS oligodendrocytes form myelin in CNS multiple flat processes of oligodendrocytes coil up to 60 axons at a time Nodes of Ranvier are present but more widely spaced White matter = regions in the brain and cord containing dense collections of myelinated fibers Gray matter = areas of mostly nerve cell bodies and unmyelinated fibers PHYS 203 Class 2 Neurophysiology neurons are highly irritable …irritable = respond to stimuli neuron stimulated…..electrical impulse generated…….impulse conducted along axon…… this response is called the Action Potential Voltage = the measure of potential energy generated by a separated charge Potential Difference / Potential = the voltage difference between 2 points greater difference = higher voltage Current = flow of electrical charge from one point to another depends on Voltage and Resistance Resistance = the hinderance to charge flow from substances through which the current passes Ohm’s Law current = voltage / resistance greater voltage (potential difference) = greater current greater resistance = smaller current plasma membranes have a slight difference in the positive and negative charges on each side --- there is a potential across the membranes Resting Membrane Potential voltage difference in the neuron vs in the extracellular fluid is -70mV inside is negative relative to outside this is called resting membrane potential and the membrane is polarized RMP is made from the differences in the ionic makeup of the ECF and ICF and the diffs in membrane permeability to those ions cell has lower Na+ and higher K+ ECF have higher Na+ and lower K+ In the ECF the + Na is balanced by Cl In the ICF the + K is balanced by negative proteins K+ plays the most important role in determining MP At rest membrane is: o impermeable to negative proteins o slightly permeable to Na o very permeable to K o freely permeable to Cl at RMP the negative inside is due to greater diffusion of K+ out than Na+ into cell Membrane Potentials that Act as Signals change in MP produces: o graded potentials – incoming short distance signals o action potentials – long-distance signals along axons Depolarization = reduction in membrane potential inside of cell becomes less negative, closer to zero or goes above zero Hyperpolarization = increase in membrane potential inside of cell becomes more negative depolarization produces nerve impulses, hyperpolarization inhibits Graded Potentials short-lived local changes in membrane potential called graded because – magnitude varies directly with stim strength stronger stimulus – greater voltage changes - further the current flows triggered by a stimulus (a change in the neurons envt) casues gated ion channels to open receptor potential = the graded potential created due to receptor of a sensory neuron being excited by heat, light etc… when depolarization occurs….. inside the cell……. K+ moves away from depol area and accumulates on neighbouring areas….there the K+ neutralizes the resting –ve charge on outer membrane…… +ve ions move towards the depolarized region since the membrane charges are reversed there and the outside is not –ve these +ves move and their spot becomes occupied by –ve ions (Cl, HCO3) therefore the outside area near the depol area becomes less positive (since the +ves were attracted to the depol spot so they move and the –ve Cl replaces its spot….becoming more –ve on the outside in that next spot) and on the inside the area becomes less negative (K+ is moving away from depol spot to next spot making that next spot more +ve or less –ve) therefore that next spot is now less –ve on the inside (closer to zero) since the inside got less negative when K+ moved towards it and the outside got more – ve when the + moved away from it so that next spot is depolarized Action Potentials method by which neurons send messages over long distances AP is brief reversal of MP from -70mV to +30 depol followed by repol and usually a short hyperpol do not decrease in strength with distance in neurons AP also called a nerve impulse voltage gated channels are opened at axon hillock due to a stimulus (Graded potential) from the dendrite and cell body membranes………membrane permeability changes sensory neurons – AP generated by the peripheral/axonal process just proximal to the receptor region PHYS 203 Class 3 - Summary Action Potential AP is brief reversal of memb potential with a total change in voltage of 100 mV from -70 to +30 Generation of AP 1. Resting State – voltage gated channels closed 2. Depolarization – increase Na permeability and reversal of memb pot depolarization = change in memb pot from –ve to +ve due to influx of Na+ 3. Repolarization – decrease Na permeability / Increase K permeability repolarization = return of cell to its negative state due to Na + influx stopping due to K+ leaving 4. Hyperpolarization – K+ permeability continues repol has restored electrical conditions …..back to -70 but resting ionic conditions are not restored Na/K pump redistributes Na and K ….3 Na out, 2 K back in…more + pumped out keeps the inside more –ve Absolute Refractory Period – when Na+ channels are open and resetting to original state, they will not respond to another stimulus …..ensures each AP is in an all or none event and enforces one-way transmission of AP Relative Refractory Period – after the ARP….most Na+ return to resting state, some K+ channels still open, repol is occurring. Threshold is higher….a stronger than normal stimulus is needed to reopen the NA+ that have returned to normal…..therefore strong stimulus can cause more frequent generation of APs. Conduction Velocity rate of propagation depends on: axon diameter: larger = faster….due to less resistance myelination: unmyelinated – continuous conduction myelinated – insulates, prevents leakage of charge and allows voltage to change fast…salutatory conduction….jumps from node to node. type A neurons – somatic sensory and motor – skin, skel musc and joints - largest diam, thick myelin sheath, fastest type B neurons – ANS motor fibers, visceral sensory, small somatic sensory - lightly myelinated, intermediate diam, medium speed type C neurons - ANS motor fibers, visceral sensory, small somatic sensory - unmyelinated, smallest diam, no salutatory, slowest The Synapse – junction that mediates info transfer from one neuron to the next Electrical Synapses protein channels connect cytoplasm of adjacent neurons and allow ions to flow from one neuron to next good means of synchronizing activity of all interconnected neurons…..very fast transmission Chemical Synapses release and receive chemical neurotransmitters made of: axon terminal of presynaptic neuron and receptor region for NT on postsynaptic neuron Synaptic Cleft separates these 2 – fluid filled space (one millionth of an inch) nerve impulse reaches axon terminal membrane depolarizes Na+ channels and voltage-gated Ca++ channels open Ca++ follows its electrochemical gradient into the terminal from ECF Ca++ directs synaptic vesicles to fuse with axon membrane vesicles empty contents into synaptic cleft Ca++ is removed from the terminal….. NT diffuses across synaptic cleft neurotransmitter binds to protein receptors on post synaptic membrane receptor changes shape ion channels in membrane open graded potential occurs Responses at Post Synaptic neuron: Excitatory Synapses and EPSPs at an excitatory synapse….NT binding causes depol of postsyn memb chemically gated ion channel opens…Na and K move in opposite directions the local graded depolarization is called EPSP EPSP helps trigger an AP distally at axon hillock Inhibitory Synapses and IPSPs binding of NT at inhibitory synapses reduces postsyn ability to generate an AP induce hyperpolarization causes membrane to become more permeable to K+ or Cl either K+ moves out or Cl- moves in this is called an IPSP Temporal Summation quick succession of impulses from presyn neuron…quick bursts of NT released Spatial Summation large numbers of terminals stimulate the neuron at the same time Axon hillock keeps track of the EPSPs and IPSPs, whichever dominates casues depolarization, hyperpolarization or nothing PHYS 203 Class 4 Neurotransmitters the means by which neurons communicate with each other Classification by Chemical Structure 1 Acetylcholine - Ach released at neuromuscular junctions once released by presyn terminal, Ach binds to postsyn receptors briefly then released and degraded to acetic acid and choline by enzyme acetylcholinesterase located in syn cleft released by neurons that stimulate skel musc and some ANS neurons, some CNS neurons release Ach too can be excitatory or inhibitory…..E at NMJ, I in cardiac muscle 2,Biogenic Amines from amino acids 1. Epinephrine released in motor neurons in the ANS (SNS) excitatory or inhibitory 2. Norepinephrine released in motor neurons in the ANS (SNS) excitatory or inhibitory 3. Dopamine released by substantia nigra in basal ganglia (motor control, cognition) excitatory or inhibitory 4. Serotonin secreted by brain stem inhibitory role in mood, attention, sleep, appetite 3. Amino Acids 1. Glycine in spinal cord inhibitory 2. GABA in spinal cord, cerebellum, hypothalamus, cortex inhibitory 3. Glutamate in spinal cord, brain stem, cortex excitatory 4. Peptides neuropeptides are strings of amino acids 1. Substance P mediates pain signals 2. Endorphins natural opiates… reduce perception of pain inhibitory – inhibits action of substance P Sensory Receptors respond to changes in their environment – stimuli Adaptation change in sensitivity in presence of a constant stimulus Phasic Receptors fast adapting pacinian and meissners quickly ignore stimulus Tonic Receptors sustained response..little or no adaptation nociceptors, proprioceptors …protective importance of their information continue to fire continuously Receptors grouped according to Stimulus Type 1. Mechanoreceptors – stimulated by touch, pressure, vibration, stretch 2. Thermoreceptors – stim by temp changes 3. Photoreceptors – respond to light energy….retina 4. Chemoreceptors – respond to chemicals in solution 5. Nociceptors – respond to damaging stimuli that result in pain Unencapsulated Dendritic endings/free/naked nerve endings 1. Merkel discs free nerve endings associated with large epidermal cells (Merkel cells) – lie in deeper layers of epidermis…function as light touch receptors tonic – slow adapting discriminative touch 2. Root Hair Plexuses / Hair Follicle Receptors free nerve endings that wrap around hair follicles…light touch receptors……detect bending of hairs…detect mosquito landing on skin…tickle Encapsulated 1. Meissner’s Corpuscles just beneath epidermis in dermal papillae numerous in sensitive and hairless areas for discriminative touch phasic…. rapid adapting 2. Pacinian corpuscles/Lamellated Corpuscles deep in dermis and subcutaneous tissue under skin in joints, tendons, muscles stimulated by deep pressure, respond only when pressure is first applied or there is a change in stimulus phasic 3. Ruffini Endings in dermis, subcutaneous tissue, joint capsules stimulated by deep continuous pressure tonic – slow adapting Phys 203 Class 5 Proprioceptors position sensors……….monitor position of joints, muscles perceive : static body posture - static position of the body as a whole, position of body parts movement of body parts in relation to others……..velocity of mvmt, duration located in skeletal muscles, tendons, joints, ligaments, CT of bones and muscles advise the brain of body movements monitor how much the organs containing these receptors are stretched monitor the strength of a muscle contraction, rate of a contraction monitor how much tension in tendons monitor change in joint position monitor position of head relative to ground they are mechanoreceptors carry info to brain and cord tonic….slow-adapting continually monitor position of body parts and coordinate movements Muscle Spindles in perimysium of muscle detect stretch in a muscle and initiate a reflex to resist the stretch (contract) Anatomy of Muscle Spindle primary sensory endings of large Type 1a fibers – innervate spindle centre stimulated by rate and degree of stretch when intrafusal fibers are stretched these sensory fibers are stretched depolarization occurs secondary sensory endings of small Type II fibers – innervate spindle ends stimulated by degree of stretch detects that a stretch happened, that’s it gamma efferent fibers - come from the spinal cord, innervate spindle ends maintain spindle sensitivity (cause the intrafusal fibers to contract when the extrafusal ones are contracting so they are not slack…keeping them taut will keep them sensitive to stretch) alpha efferent fibers - come from the spinal cord stimulate the extrafusal fibers to contract How Does the Muscle Spindle Work? at rest, Ia and II fibers are tonically active monitoring body position they are constantly firing (espec in postural muscles) and stimulating alpha motor neurons to stimulate extrafusal fibers to contract to maintain muscle tone intrafusal fibres (Ia and II) get stretched as whole muscle is stretched…..Ia and II fibers fire more rapidly than normal……stimulate alpha motor neuron in cord…cause the extrafusal fibers to contract and relieve the stretch Golgi tendon organ in tendons bundles of collagen enclosed in a capsule with sensory terminals coiling around tendon is stretched when muscle contracts…..nerve endings are compressed and then activated causes muscle relaxation and lengthening in response to tension golgi tendon organs……..monitor the amount of tension in the muscle muscle spindles………..monitor the length of the muscle How does the Golgi Tendon Organ Work? muscle tension increases substantially during contraction tendon is stretched nerve endings/GTO are compressed afferent impulses to cord impulses to cerebellum integration synapse with alpha motor neurons alpha motor neurons are inhibited motor neurons inhibit the contracting muscle, muscle relaxes and antagonist is activated to contract….reciprocal activation PHYS 203 Class 6 Reflexes Some important reflexes a. stretch reflex b. tendon reflex c. flexor-withdrawal reflex d. crossed extensor reflex 1. Stretch Reflex monosynaptic ipsilateral respond to muscle stretch, muscle contraction occurs steps involved in stretch reflex quick stretch of muscle occurs…….reflex hammer muscle spindle is stretched muscle spindle activated spindle generates AP AP travels along afferent fiber through dorsal root of spinal cord into posterior aspect of spinal cord synapses with an alpha motor neuron in cord….motor neuron body in anterior horn EPSP triggered, impulse along alpha motor neuron axon impulse arrives at NMJ, Ach released Ach binds to extrafusal muscle cell signals muscle AP and contraction muscle shortens, relieves stretch Reciprocal Inhibition sensory neuron synapses with an inhibitory interneuron inhibits the motor neuron innervating the antagonistic muscle….hamstrings hams will relax so that quads can contract antagonists then relax so they don’t resist the shortening of the stretched muscle 2. Tendon Reflex disynaptic ipsilateral response to muscle tension, muscle relaxation occurs steps involved in tendon reflex muscle tension increases substantially during contraction tendon is stretched, nerve endings/GTO are compressed afferent impulses to cord integration – synapse with inhibitory interneuron synapse with alpha motor neurons alpha motor neurons are inhibited due to IPSP motor neurons inhibit the contracting muscle, muscle relaxes and antagonist is activated to contract….reciprocal activation Reciprocal Activation sensory neuron synapses with another interneuron…excitatory interneuron that interneuron synapses with another motor neuron…causes EPSP antagonistic muscle contracts so….. with stretch reflex…EPSP to muscle to contract (quads) IPSP to antagonist to relax it (hams) with tendon reflex …. IPSP to muscle to relax it (quads) EPSP to antagonist to contract it (hams) 3. Flexor Withdrawal Reflex polysynaptic (several muscles may be involved to move limb) ipsilateral protective causes withdrawl of body part from painful stimulus EPSPs and IPSPs sent to several motor neurons….called intersegmental reflex arc 4. Crossed Extensor Reflex polysynaptic contralateral occurs in conjunction with Flexor Withdrawal reflex in weight bearing limbs ipsilateral withdrawal reflex combined with a contralateral extensor reflex sensory neurons synapse with interneurons (EPSP and IPSP) on same side of body and with excitatory interneuron controlling extensor muscles on opposite side of body Assessing neuromuscular function Dermatomes dermatome = area of skin innervated by a single spinal nerve some overlapping occurs…about 50%....therefore destruction of a single spinal nerve will not result in complete numbness anywhere C5-T1 supply the skin of upper limbs thoracic nerves supply thorax lumbar nerves supply anterior thighs and legs sacral nerves supply posterior lower legs Myotomes myotome = muscles supplied by motor neurons of a spinal segment Clinical Reflexes show intact sensory and motor connections Patellar Reflex - quads contract, knee extends.....tests L2 L3 L4 Achilles - gastrocs contract, ankle plantar flexes.....tests L5 S1 S2 Biceps - biceps contract, elbow flexes....tests C5 C6 Brachioradialis - brachioradialis contracts.....tests C5 C6 Triceps - triceps contract, elbow extension.....tests C7 C8 Superficial Reflexes elicited by gentle cutaneous stimulation depend on upper motor neuron pathways and spinal cord level reflex arcs Plantar Reflex tests integrity of L4-S1 cord levels and tests the function of the corticospinal tracts (UMN paths) draw a blunt object along plantar surface of foot from toe to heel normal response – curl toes abnormal response – big toe dorsiflex and other toes fan out laterally (Babinski sign) Abdominal Reflex tests integrity of T8-T12 cord levels stroke skin of lateral abdomen above to the side or below the umbilicus normal response – contraction of abdominal muscles causing umbilicus to move toward stroked area Phys Class 7 Spinal cord function of cord: reflexes integration path for sensory and motor impulses Spinal Nerves 31 pairs Nerve Roots Dorsal Root o posterior root o sensory fibers from periphery running into cord o cell bodies are located at dorsal root ganglion Ventral Root o anterior root o motor fibers from brain/cord sending info to periphery o cell bodies are inside spinal cord in anterior horn of gray matter Organization of the Cord Gray Matter neuron cell bodies of interneurons (that have synapsed with incoming sensory neurons) neuron cell bodies of motor neurons (that have synapsed with interneurons or sensory neurons) unmyelinated axons dendrites Lateral Masses each lateral mass has horns – dorsal, ventral, lateral posterior horn contain cell bodies of interneurons (sensory info coming in from periphery via dorsal horns and synapsing with interneurons cell bodies in dorsal horn (or motor neuron bodies in the case of reflexes) anterior horn contain cell bodies of somatic motor neurons sending message out from cord along motor nerve to muscle Gray Commissure connects the lateral masses Lateral Horns cell bodies of SNS motor neurons to viscera SNS motor axons from lateral horn join the somatic motor axons from the ventral horn to exit out the ventral horn of the cord Zones of Gray Matter somatic sensory area - contains interneuron cell bodies receiving info from somatic sensory neurons from the periphery visceral sensory area - contains interneuron cell bodies receiving info from visceral sensory neurons from the periphery somatic motor area - contains cell bodies of somatic motor neurons innervating skeletal muscles, receiving info via synapse with interneurons from brain or sensory neurons axon will leave cord via ventral horn and run to skeletal muscle visceral motor area - contains cell bodies of visceral motor neurons innervating viscera, receiving info via synapse with interneurons from brain or sensory neurons axon, will leave cord via ventral horn and run to viscera Phys Class 8 Spinal tracts White Matter ascending tracts = up = sensory info descending tracts = down = motor info – from brain or other areas of cord commissural tracts = transverse – across from one side of cord to other general rules of tracts 1. All are paired – on the left and right 2. Most cross over from one side of cord to other…decussate 3. Most are chains of 2 or 3 neurons 4. Most exhibit somatotopy Somatotopy spatial relationship among the tract fibers that reflects the orderly mapping of the body ex. tracts with sensory info from the upper body lie lateral to tracts with info from the lower body Ascending Tracts 3 main ascending pathways 1. Nonspecific formed by lateral spinothalamic and anterior spinothalamic tracts cross over occurs in spinal cord pain, temp, coarse touch – sensations we are aware of but have difficulty localizing precisely on the body surface anterior spinothalamic – crude touch and pressure lateral spinothalamic – pain and temperature info goes to somatosensory cortex to give conscious awareness of sensation lesion – loss of pain, temp, light touch on contralateral side below level of lesion 2. Specific mediate precise transmission of inputs from a single type of sensory receptor that can be localized precisely on the body surface discriminative touch, vibration, proprioception, fine touch fasciculus gracilis – info from lower body…..below T6 … to medulla fasciculus cuneatus – info from upper body….above T6 … to medulla the medial leminiscus – medulla to thalamus info crosses at medulla info then goes to somatosensory cortex on contralateral side lesion – loss of poprioception, discriminative touch ipsilaterally below lesion (because crossover is in the brain) 3. Spinocerebellar anterior posterior proprioception info from lower limbs and trunk to cerebellum (motor coordination, fine tune motor movements)…..info from muscle spindles, GTO coordinates skeletal muscle activity ipsilaterally posterior does not decussate anterior decussates twice – at cord and pons lesion – poor coordination ipsilaterally, awkward posture and gait nonspecific pathway o temperature receptor o 1st order sensory neuron enters dorsal horn of cord o synapses with 2nd order interneuron o crosses to other side of cord and from dorsal to anterior o ascends cord via spinothalamic tract (anterior or lateral) o synapse in thalamus with 3rd order interneuron o travels to somatosensory cortex specific pathway o touch receptor o 1st order sensory neuron enters dorsal horn of cord o ascends cord via gracilis (lower body) or cuneatus (upper body) o synapse in medulla with 2nd order interneuron o interneuron crosses to other side o travels to thalamus via medial leminiscal tract o synapse with 3rd order interneuron o travels to somatosensory cortex spinocerebellar pathway o muscle spindle o 1st order sensory neuron enters dorsal horn of cord o synapse with 2nd order neuron o ascends to cerebellum efferent impulses from brain to cord direct pathways – pyramidal tracts indirect pathways – all others pathways involve 2 neurons…..an upper motor neuron and a lower motor neuron upper motor neurons: pyramidal cells of motor cortex subcortical motor nuclei lower motor neurons: anterior motor horn nulei UMN = neuron above the synapse LMN = neuron below the synapse Direct Pathways aka Pyramidal tracts , aka corticospinal tracts voluntary muscle activity from pyramidal neurons in the primary motor cortex called direct because the axons descend without synapsing from cortex to cord synapse with : interneurons that influence motor neurons directly with anterior horn motor neurons anterior horn neuron stimulated….causes activation of skeletal muscle lateral corticospinal crosses over at medulla then continues down cord to synapse with anterior horn motor neuron then exit to periphery anterior corticospinal crosses at spinal cord level at where they synapse with anterior horn motor neuron and then exit to periphery Indirect Pathways aka Extrapyramidal Tracts (“extra to”/indirect/multineuronal) programmed automatic movements , maintain skeletal muscle tone, balance, posture, visual/auditory tracking, coordinate body movements rubrospinal controls muscle tone – distal limb flexor muscles from red nuclei of midbrain fibers cross just below red nuclei down lateral columns reticulospinal controls cardiovascular and respiratory regulation, muscle tone, many basic functions such as sleep, eating from reticular formation in pons and medulla motor impulses to muscles controlling muscle tone, visceral functions has crossed and uncrossed fibers cardiovascular/respiratory viscera sends sensory info to reticular formation in pons and medulla (brain stem), synapse with efferent interneurons that travel down reticulospinal tract, may or may not cross over, synapse with an anterior horn motor neuron which exits the cord to stimulate cardiovascular or respiratory viscera tectospinal visual and auditory reflexes, coordinates movement of eyes/head to visual input in anterior white columns from superior colluliculi of midbrain (visual reflex centre) visual/auditory stimuli sends sensory info into superior colliculus in midbrain, synapse with efferent interneurons that travel down tectospinal tract, cross over in the cord, synapse with an anterior horn motor neuron which exits the cord to stimulate skeletal muscle vestibulospinal balance, maintain muscle tone, activate limb and trunk extensors anterior white columns from vestibular nuclei of medulla do not cross vestibular labyrinth in inner ear sends impulses along cranial nerve 8 to vestibular nuclei in medulla (info about balance), synapse with efferent interneurons, impulses then travel along interneurons down vestibulospinal tract to synapse with anterior horn motor neuron, which exits the cord to stimulate muscles to maintain muscle tone, balance etc. Upper Motor Neuron Disorders spastic paralysis- spinal motor neurons are intact, muscles are stimulated irregularly by spinal reflexes…muscles remain healthy longer but the movements are no longer voluntary….they are spastic…the muscles become permanently shortened CP, brain injuries, spinal cord injuries, MS, stroke hyperreflexia Lower Motor Neuron Disorders message sent from brain but motor neurons innervating muscle are absent flaccid paralysis hyporeflexia atrophy Descending Tract Diseases ALS motor neuron disease – UMN and LMN destruction of ventral horn motor neurons and pyramidal tracts lose muscle tone and ability, lose speak, swallow….. die within 5 years cause unknown Polio destruction of ventral horn motor neurons by poliovirus LMN disorder paralysis and atrophy recovered survivors may experience lethargy, burning pain, weakness, atrophy…postpolio syndrome Phys 203 Class 9 The Brain basic divisions: 1. cerebral hemispheres – cortex (motor, sensory, association areas), white matter, basal ganglia 2. diencephalon – hypothalamus, thalamus, epithalamus 3. brain stem- midbrain, pons and medulla 4. cerebellum Ventricles continuous with central canal of cord hollow chambers filled with CSF, lined by ependymal cells lateral ventricles – in each cerebral hemisphere third ventricle – narrow, in diencephalons fourth ventricle – in hindbrain behind pons and medulla Cerebral Hemispheres superior part of brain elevated ridges = gyri shallow grooves = sulci deep grooves = fissures lobes: frontal, parietal, temporal, occipital, insula (under temporal) Cerebral Cortex conscious mind, awareness, communication, memory, comprehension, voluntary movements brain is mapped by function: specific motor areas, specific sensory areas, association areas, other areas for memory, language etc… all neurons are interneurons, not sensory or motor (the info is sensory or motor) each hemisphere controls opposite side of body the hemis are not equal in function – lateralization/specialization of cortical functions Motor Areas 1. Primary (somatic) motor cortex 4 precentral gyrus pyramidal cells (large neurons) axons form the pyramidal/corticospinal tracts, run down cord to control voluntary movements motor homunculus – diagram showing the relative amount of cortical tissue devoted to each function…areas of precise motor control (face, tongue, hands) have more neurons devoted to them and are larger represented 2. Premotor Cortex 6 anterior to precentral gyrus controls learned motor skills of a repetitive or patterned nature ex. playing instrument coordinates several muscle groups by activating primary motor cortex informs primary motor area of what motor neurons to activate to perform certain movements 3. Broca’s area anterior to premotor cortex motor speech area – directs muscles involved in speech production controls movement of tongue, lips etc… lesion here = motor aphasia - loss of ability to produce language Wernickes area - processing of language lesion here – sensory aphasia - ability to speak is fine but use incorrect words damage area of primary motor cortex – paralysis of muscle controlled by the specific area...loss of voluntary mvmt, reflexes are ok damage to premotor cortex – loss of the motor skill in that corresponding region, muscle strength is ok. ex. typing speed would decrease, you can still make those specific type of movements but the skill can be reprogrammed into another set of premotor neurons with practice just like the initial learning process. Sensory Areas 1. Primary somatosensory cortex postcentral gyrus of parietal lobe receive info from somatic sensory receptors , proprioceptors neurons being stimulated reflect the body region being stimulated somatosensory homunculus – diagram showing amount of sensory cortex devoted to a particular body region based on that region’s sensitivity 2. Somatosensory association cortex posterior to primary somatosensory cortex integrate sensory inputs from primary sensory cortex, to produce an understanding of what the stimulus is – size, texture, etc. draws upon memories of past sensory experiences 3. Visual Areas primary visual cortex o posterior tip of occipital lobe o info from retina o somatotopy – areas in visual field are systematically organized on visual cortex left visual field is on right visual cortex and right on left, sup and info opposite also visual association areas o covers much of the occipital lobe o uses past visual experience to interpret visual stimuli allowing recognition and appreciation of what is being seen o prosapagnosia – inability to recognize faces 4. Auditory Areas primary auditory cortex o info from hearing receptors in ear, interpret pitch loudness, location auditory association areas o perception of sound that we hear…speech, thunder etc.. o memories of sound help interpret what is heard 5. Olfactory Cortex info from receptors in superior nasal cavities, conscious awareness of odors has connections to memory and emotion….connected to smells/part of limbic system 6. Gustatory Cortex insula (deep to temporal lobe) perception of taste stimuli PHYS 203 Class 10 Brain II Association areas areas that receive inputs from many senses and send outputs to many areas gives meaning to info received stores info in memory, ties it to previous experience and knowledge decides what action to take relays info to premotor cortex premotor cortex communicates with primary motor cortex 1. Anterior Association area / Prefrontal Cortex frontal lobe intellect, complex learning (cognition), personality, recall abstract ideas, judgement, reasoning, planning 2. Posterior Association area / Gnostic Area temporal, parietal and occipital lobes interprets all sensory info of a particular situation, generates understanding of the situation, sends info to prefrontal cortex to add emotion and intellect and determine a response 4. Lauguage Area / Wernickes Area temporal lobe interpretation of speech lesion = receptive aphasia…..can hear but cant understand, can speak but words do not make sense because they can not interpret what they are saying 5. Visceral Association insula perception of visceral stimuli Cerebral White Matter communication between cerebral areas and between cortex and lower CNS areas commissures – connect corresponding gray areas of the 2 hemis corpus callosum – largest association fibers – connect diff parts of same hemi projection fibers – travel vertically from lower areas to cerebrum or from cortex down internal capsule – band formed by projection fibers at top of brain stem corona radiata – fanning/radiating of tracts above the capsule Basal Nuclei caudate nucleus, putamen, globus pallidus receive input from cerebral cortex, other subcortical nuclei role in motor control, starting, stopping, monitoring intensity of movement inhibit unnecessary movements, help perform several actions at once as a group also called corpus striatum because the fibers of internal capsule pass by them and make it look striped Parkinsons destruction of substantia nigra – nuclei in midbrain that communicates with basal ganglia to control movement insufficient dopamine production results in altered/reduced input to basal ganglia from substantia nigra and motor cortex……the excitatory pathways are inhibited and the inhibitory pathways are excited between the basal ganglia and the cortex. result is altered movement….rigidity, tremor, movements that should be inhibited are not and movements that are excitatory are inhibited Huntingtons Chorea mutant protein in brain cells causes neuron death….leaves holes in the brain inhibitory pathway of basal ganglia degenerated…thalamus no longer inhibits and smooths the movements…….basically crossed mixed up paths and therefore jerky uncontrolled movements Hemiballism damage to subthalamic nuclei causes reduction of inhibitory output on the thalamus, and this disinhibition gives rise to excessive excitatory drive to the cortex, which is expressed as contralateral movements Athetosis slow repetitive writing movements Diencephalon Thalamus afferent impulses from all senses synapse here for crude recognition of the stimuli similar impulses are relayed as a group from here via internal capsule to sensory cortex and sensory association areas impulses from all areas of brain so that sensory info can be integrated and evoke the appropriate reaction…..motor response, automatic movements… Hypothalamus contains many nuclei visceral control centre vital role in homeostasis homeostatic roles: 1. Antonomic control centre 2. Emotional response 3. Body temperature regulation 4. Regulation of food intake 5. Regulation of water balance and thirst 6. Regulation of sleep/wake cycles 7. Control endocrine system functioning Epithalamus contains pineal gland – secretes melatonin – sleep inducing signal, along with hypothalamic nuclei regulates sleep/wake The Brain III Brain Stem – Mibdrain, Pons, Medulla produce programmed automatic survival behaviours Midbrain cerebral peduncles – corticospinal/pyramidal tracts cerebellar peduncles – tracts connecting midbrain to cerebellum superior colliculi – visual reflex centres inferior colliculi – auditory relay to cortex and auditory reflex red nucleus – red…blood, iron…relay neclei in some descending motor paths that effect limb flexion (rubrospinal) Pons conduction tracts between cord and cortex and cerebellum and cortex Medulla inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum cochlear nuclei – auditory relay vestibular nuclei – vestibular (equilibrium) relay nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending somatic sensory info heading to somatosensory cortex visceral motor nuclei: cardiovascular centre - cardiac centre (HR), vasomotor (BP) respiratory centre - control rate and depth of breathing other centres - hiccupping, swallowing, coughing, sneezing hypothalamus controls visceral functions by relaying its instructions through medullary centres which carry them out Cerebellum processes inputs from cerebral motor cortex, brain stem nuclei, sensory receptors to provide precise timing and appropriate patterns of skeletal muscle contraction for smooth coordinated movements subconscious equilibrium inputs here to adjust posture and maintain balance motor cortex via relay nuclei in stem notify cerebellum of intent to initiate voluntary muscle contraction Functional Brain Systems Limbic System septal nuclei, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus, amygdale, hypothalamus, anterior thalamic nuclei emotional brain communicates with cerebral cortex creating relationship between feelings (limbic) and thoughts (cortex) Reticular Formation governs brain arousal reticular activating system – a group of neurons that send continuous impulses to cortex…keeps cortex alert ascending sensory tracts synapse with RAS which enhances their arousing effect on the cortex sensory inputs are filtered here reticulospinal tracts control skeletal muscle and some visceral motor functions PHYS 203 Class 12 Autonomic Nervous System Differences in somatic and autonomic NS Effectors somatic – skeletal muscles ANS – cardiac, smooth muscle, glands Efferent Pathways somatic – motor neuron bodies in CNS, axons run in spinal or cranial nerve to skeletal muscle ANS – 2 neuron chain - preganglionic neuron and post ganglionic neuron Neurotransmitter Effects somatic – release Ach – excitatory ANS – SNS and PSNS pregang neuron release Ach SNS postgang release norepi on to the effector PSNS postgang release Ach onto the effector excitatory or inhibitory response depends on receptor type on effector organ SNS and PSNS innervate the same viscera but cause opposite responses – balance each other SNS is generally excitatory (but not ALWAYS) PSNS is generally inhibitory (but not ALWAYS) Sympathetic Nervous System fight or flight response fast HR, dry mouth, cold sweaty skin, dilated pupils During exercise: increase blood flow to muscles – visceral constriction of vessels increase lung ventilation – bronchioles dilate..increases oxygen and delivery to cells liver releases more glucose into blood nonessential activities are damped…GI motility slows SNS neurons originate from thoracolumbar areas of CNS preganglionic neurons synapse in sympathetic chain near spinal cord intake Parasympathetic Nervous System rest and digest state digestion – good idea to relax after eating….so digestion is not interfered with by SNS activity keeps BP, HR, respiration rate low, high digestive rate, pupils constricted PSNS neurons originate from the cranial and sacral areas of CNS preganglionic neurons synapse in ganglia located close or in organs Differences in SNS and PSNS PSNS neurons originate from brain and sacral areas of cord SNS neurons originate from thoracolumbar areas PSNS has long preganglionic and short postganglionic fibers SNS has short preganglionic and long postganglionic fibers PSNS ganglia are located in visceral effector organ SNS ganglia are close to spinal cord visceral sensory neurons – chemical changes, stretch, irritation of viscera visceral reflex – receptor, sensory neuron, integration centre, motor neuron, effector …but has 2 chain motor neuron (pregang and post gang neurons) referred pain since visceral pain afferents travel the same paths as somatic pain fibers… pain stimuli arising in the viscera can be perceived as arising in somatic areas Specific SNS functions: 1. controls vascular smooth muscle causes dilation or constriction of vessels increased tone in these muscles causes constriction of vessel… ..decreased flow to tissue decreased tone in these muscles causes dilation of vessel…..increased flow to tissue 2. thermoregulation SNS mediates reflexes that regulate body temp via constriction and dilation of blood vessels ex. core temp increases – skin blood vessels dilate, skin is flushed with warm blood, heat near surface of skin will radiate away from body and cool the body ex. core temp falls – skin vessels are constricted so that blood stays in deeper vital organs 3. stimulates renin release in kidneys renin is an enzyme that promotes increase BP by acting on the kidneys to increase water retention and therefore BP 4. Metabolic effects increases metabolic rate increases blood glucose – breakdown stored glycogen in liver increases lipolysis – breakdown fat to use to make ATP Control of Autonomic Functioning hypothalamus is the integrative centre orders from there flow through lower brain centres cortex and limbic system can influence ex. a memory of a frightening experience makes your heart race, thinking of food makes your mouth water The Brain basic divisions: 1. cerebral hemispheres - cortex, white matter, basal nuclei 2. diencephalon - thalamus, hypothalamus, epithalamus 3. brain stem - midbrain, pons and medulla 4. cerebellum Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei Cerebral Cortex awareness, communication, memory, voluntary movements Primary (somatic) motor cortex control voluntary movements Premotor Cortex controls learned motor skills of a repetitive or patterned nature ex. playing instrument Broca’s area motor speech area – directs muscles involved in speech production Frontal eye field controls voluntary movements of eyes Primary somatosensory cortex receive info from somatic sensory receptors, proprioceptors Somatosensory association cortex integrate sensory inputs from primary sensory cortex, to produce an understanding of what the stimulus is – size, texture, etc. Visual Areas primary visual cortex - info from retina visual association areas - uses past visual experience to interpret visual stimuli allowing recognition and appreciation of what is being seen Auditory Areas primary auditory cortex - info from hearing receptors in ear, interpret pitch loudness, location auditory association areas - perception of sound that we hear Olfactory Cortex info from receptors in superior nasal cavities conscious awareness of odors Gustatory Cortex perception of taste stimuli Visceral Sensory Area conscious perception of visceral sensations – upset stomach, full bladder Vestibular cortex conscious awareness of balance Multimodal Association areas areas that receive inputs from senses and send outputs to many areas gives meaning to info received stores info in memory, ties it to previous experience and knowledge relays info to premotor cortex, which communicates with primary motor cortex 3 major association areas Anterior Association area intellect, complex learning (cognition), personality, judgment, reasoning Posterior Association area recognizing patterns, faces, localize surroundings, bind different sensory inputs into a whole Limbic Association area emotional impact lateralization = unique abilities specific to each hemi not shared by the other cerebral dominance = the hemisphere that is dominant for language….90% of people it is the left…right handed Cerebral White Matter communication between cerebral areas and between cortex and lower CNS areas commissures – connect corresponding gray areas of the 2 hemis corpus callosum – largest commissure association fibers – connect diff parts of same hemi projection fibers – travel vertically from to or from cortex internal capsule – band formed by projection fibers at top of brain stem corona radiata – fanning/radiating of tracts above the capsule Basal Nuclei caudate nucleus putamen globus pallidus receive input from cerebral cortex and other subcortical nuclei some role in motor control, attention, cognition starting, stopping, monitoring intensity of movement inhibit unnecessary movements, help perform several actions at once as a group also called corpus striatum because the fibers of internal capsule pass by them and make it look striped Diencephalon – Thalamus, Hypothalamus, Epithalamus Thalamus afferent impulses from all senses synapse here sensory information is edited here crude recognition of sensation occurs here ie. pleasant or unpleasant. Hypothalamus contains many nuclei for visceral control and homeostasis homeostatic roles: 1. Autonomic control centre - BP, HR, digestive motility, pupil size 2. Emotional response - perceives pleasure, fear, rage, acts through ANS 3. Body temperature regulation - receives input from thermoreceptors 4. Regulation of food intake - responds to blood levels of nutrients 5. Regulation of water balance and thirst - osmoreceptors 6. Regulation of sleep/wake cycles - suprechiasmatic nucleus 7. Control endocrine system functioning - releasing hormones Epithalamus contains pineal gland – secretes melatonin – sleep inducing signal Brain Stem – Mibdrain, Pons, Medulla produce programmed automatic survival behaviours Midbrain cerebral peduncles – corticospinal/pyramidal tracts cerebellar peduncles – tracts connecting midbrain to cerebellum superior colliculi – visual reflex centres inferior colliculi – auditory relay to cortex and auditory reflex red nucleus – red…blood, iron…relay neclei in some descending motor paths that effect limb flexion (rubrospinal) Pons conduction tracts between cord and cortex and cerebellum and cortex Medulla inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum cochlear nuclei – auditory relay vestibular nuclei – vestibular (equilibrium) relay nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending somatic sensory info heading to somatosensory cortex visceral motor nuclei: cardiovascular centre - cardiac centre (HR), vasomotor (BP) respiratory centre - control rate and depth of breathing other centres - hiccupping, swallowing, coughing, sneezing hypothalamus controls visceral functions by relaying its instructions through medullary centres which carry them out Cerebellum processes inputs from cerebral motor cortex, brain stem nuclei, sensory receptors to provide precise timing and appropriate patterns of skeletal muscle contraction for smooth coordinated movements subconscious equilibrium inputs here to adjust posture and maintain balance motor cortex via relay nuclei in stem notify cerebellum of intent to initiate voluntary muscle contraction Functional Brain Systems Limbic System septal nuclei, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus, amygdale, hypothalamus, anterior thalamic nuclei emotional brain communicates with cerebral cortex creating relationship between feelings (limbic) and thoughts (cortex) Reticular Formation govern brain arousal reticular activating system – a group of neurons that send continuous impulses to cortex…keeps cortex alert ascending sensory tracts synapse with RAS which enhances their arousing effect on the cortex sensory inputs are filtered here reticulospinal tracts control skeletal muscle and some visceral motor functions The Brain 1. Cerebral Hemispheres a. Cerebral Cortex Motor Areas: Primary (somatic) motor cortex Premotor Cortex Broca’s area Frontal eye field Sensory Areas: Primary somatosensory cortex Somatosensory association cortex Visual Areas primary visual cortex visual association areas Auditory Areas primary auditory cortex auditory association areas Olfactory Cortex Gustatory Cortex Visceral Sensory Area Vestibular cortex Multimodal Association areas Anterior Association area Posterior Association area Limbic Association area b. Cerebral White Matter c. Basal Nuclei 2. Diencephalon Thalamus. Hypothalamus Epithalamus 3. Brain Stem Midbrain Pons Medulla 4. Cerebellum 5. Functional Brain Systems Limbic System Reticular Formation The Brain Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei 1. Cerebral Cortex awareness, communication, memory, voluntary movements Primary (somatic) motor cortex - control voluntary movements Premotor Cortex - controls learned motor skills of a repetitive or patterned nature Broca’s area - motor speech area – directs muscles involved in speech production Primary somatosensory cortex - receives info from somatic sensory receptors, proprioceptors Somatosensory association cortex - produces an understanding of what the stimulus is Visual Areas primary visual cortex - info from retina visual association areas - uses past visual experience to interpret visual stimuli allowing recognition and appreciation of what is being seen Auditory Areas primary auditory cortex - info from hearing receptors in ear - pitch loudness, location auditory association areas - perception of sound that we hear Olfactory Cortex info from receptors in superior nasal cavities, conscious awareness of odors Gustatory Cortex perception of taste stimuli Visceral Sensory Area conscious perception of visceral sensations – upset stomach, full bladder Anterior Association area / Prefrontal Cortex intellect, complex learning (cognition), personality, judgment, reasoning Posterior Association area / Gnostic Area interprets all sensory info of a particular situation, generates understanding of the situation, sends info to prefrontal cortex Lauguage Area / Wernickes Area interpretation of speech Visceral Association perception of visceral stimuli 2. Cerebral White Matter communication between cerebral areas and between cortex and lower CNS areas 3. Basal Nuclei caudate nucleus, putamen, globus pallidus role in motor control, starting, stopping, monitoring intensity of movement inhibit unnecessary movements Diencephalon – Thalamus, Hypothalamus, Epithalamus Thalamus afferent impulses from all senses synapse here, sensory information is edited here Hypothalamus contains many nuclei for visceral control and homeostasis 1. Autonomic control centre - BP, HR, digestive motility, pupil size 2. Emotional response - perceives pleasure, fear, rage, acts through ANS 3. Body temperature regulation - receives input from thermoreceptors 4. Regulation of food intake - responds to blood levels of nutrients 5. Regulation of water balance and thirst - osmoreceptors 6. Regulation of sleep/wake cycles - suprechiasmatic nucleus 7. Control endocrine system functioning - releasing hormones Epithalamus contains pineal gland – secretes melatonin – sleep inducing signal Brain Stem – Mibdrain, Pons, Medulla produce programmed automatic survival behaviours Midbrain cerebral peduncles – corticospinal/pyramidal tracts cerebellar peduncles – tracts connecting midbrain to cerebellum superior colliculi – visual reflex centres inferior colliculi – auditory relay to cortex and auditory reflex red nucleus – red…blood, iron…relay neclei in some descending motor paths that effect limb flexion (rubrospinal) Pons conduction tracts between cord and cortex and cerebellum and cortex Medulla inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum cochlear nuclei – auditory relay vestibular nuclei – vestibular (equilibrium) relay nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending somatic sensory info heading to somatosensory cortex visceral motor nuclei: cardiovascular centre - cardiac centre (HR), vasomotor (BP) respiratory centre - control rate and depth of breathing other centres - hiccupping, swallowing, coughing, sneezing hypothalamus controls visceral functions by relaying its instructions through medullary centres which carry them out Cerebellum provides precise timing and appropriate patterns of skeletal muscle contraction for smooth coordinated movements, subconscious Functional Brain Systems Limbic System emotional brain, communicates with cerebral cortex creating relationship between feelings (limbic) and thoughts (cortex) Reticular Formation govern brain arousal, keeps cortex alert Muscular Physiology I Types of Muscle Tissue 1. Skeletal 2. Cardiac 3. Smooth 1. Skeletal striated voluntary function – body mobility 2. Cardiac striated involuntary function – pumps blood through heart 3. Smooth nonstriated involuntary function – force fluid and substances through internal body channels Functional Characteristics Excitability ability to receive and respond to stimuli (a change in environment) Contractility ability to shorten forcibly when stimulated Extensibility ability to be stretched Elasticity ability to recoil to resting length after being stretched Muscle Functions 1. Produces Movement skeletal – locomotion, manipulation cardiac and smooth – moves blood and other substances through heart and other organs 2. Maintains Posture muscles contract to make adjustments in posture to counteract gravity 3. Stabilizes Joints 4. Generates Heat occurs as muscles contract, vital for maintaining body temp Gross Anatomy made of muscle fibers, blood vessels, nerve fibers, connective tissue Connective Tissue supports each muscle cell and reinforces the muscle as a whole Endomysium – wraps muscle fiber Perimysium – wraps fascicles…..groups of fibers form a fascicle Epimysium – wraps whole muscle Microscopic Anatomy plasma membrane = sarcolemma cytoplasm = sarcoplasm numerous granules of stored glycogen lots of myoglobin – stores oxygen Myofibrils bundles of myofilaments – actin and myosin…contractile units of the muscle……thousands in a fiber sarcomeres – small sections/divisions of myofibril created due to the arrangement of actin and myosin filaments A band – area containing thick and thin filaments…dark band H zone – lighter stripe in centre of A band – thick filaments only M line – in middle of H zone – anchors the thick filaments I band – area containing thin filaments only…light band Z line – in middle of I band – anchors the thin filaments - protein Sarcomere = region between 2 Z discs Z…I….A….H…M…H…A…I…Z functional unit of muscle arranged end to end Thick Filament made of protein myosin myosin is made of a tail of 2 interwoven polypeptide chains and 2 flexible hinged heads the heads will connect to a thin filament and swivel during muscle contraction each one is surrounded by 6 thin filaments Thin Filament made of actin mostly actin is 2 intertwined long chains of connected globular units also in the thin filament: tropomyosin and troponin – control the myosin interaction with actin during a muscle contraction Sarcoplasmic Reticulum elaborate smooth ER, surrounds myofibril, forms large channels at A-I junction – terminal cisternae SR stores calcium and releases it when the muscle fiber is stimulated to contract Transverse Tubules elongated tube of sarcolemma penetrating into cell interior at A-I jctn - AP travels deep inside fiber, signals Ca release from terminal cisternae Triad T-tubule and 2 terminal cisternae Muscular Physiology II Principles of Muscle Contraction 1. Filaments do not change length……..the slide 2. Z lines move closer together…..myosin pulls actin towards centre of sarcomere 3. I bands shorten 4. H zones shorten or disappear 5. A bands move closer together, they do not change length 6. zones of overlap get larger Sliding Filament Theory - during contraction the thin filaments slide past the thick filaments so the actin and myosin overlap to a greater degree Steps of Muscle Contraction 1. Myosin attaches to actin binding site on actin is exposed, myosin head binds myosin head is in its high energy state, holding the potential energy that came from breaking the bond in ATP, ADP and P remain bound to myosin head. 2. Powerstroke ADP and P are released from myosin….allows myosin head to move the potential energy that was released from the splitting of ATP is now used and that head moves…..head changes from high energy state to low energy state as it pulls the thin filament towards the centre of the sarcomere 3. Myosin detaches new ATP binds to myosin head myosin detaches from actin myosin is still in low energy state 4. Cocking of Myosin Head ATP is split by ATPase enzyme on myosin head…split into ADP and P the energy is released to put the myosin head into the high energy state a single powerstroke from all XBs causes 1% shortening muscle can shorten by 30% Rigor Mortis - RM occurs basically because calcium is dumped into the cytoplasm causing XBs to form but then they cannot detach because there is no ATP and therefore do not allow relaxation of the muscle Tropomyosin - covers myosin binding sites on actin….covered when no Ca present Troponin - controls position of tropomyosin Excitation Contraction Coupling - ECC is the transmission of the AP and the subsequent sliding of the filaments AP along motor neuron axon axon terminal Ach released across synaptic cleft Ach binds to receptor on sarcolemma ot motor end plate depolarization of sarcolemma AP travels in all directions AP transmission along sarcolemma and down T-tubules terminal cisternae of SR activated to release Ca into sarcoplasm Ca bind to troponin troponin complex changes shape moves tropomyosin off the binding site on actin myosin binds to actin in its high energy state with ADP and P attached still ADP and P are released and the head moves and pulls the actin new ATP binds and myosin detaches in its low energy state ATP is split to provide energy for the next powerstroke and head is cocked Ca is constantly being taken back into SR so since AP is so brief, it does not take long for more Ca to be taken up then is being released not enough Ca left in sarcoplasm to bind to troponin tropomyosin blockade forms again troponin returns to original state Muscular Physiology III Review Sliding Filament steps 1-4 1. Myosin attaches to actin Ca++ (that was relased from SR into sarcoplasm) has already bound to troponin, pulled tropomyosin off the binding site, myosin binds to actin ATP was previously split to ADP and P which are still bound to the myosin head myosin head is in its high energy state, holding the potential energy that came from breaking the bond in ATP. myosin head is extended and waiting to move 2. Powerstroke ADP and P are released from myosin….allows myosin head to move the potential energy that was released from the splitting of ATP is now used and that head moves…..head changes from high energy state to low energy state as it pulls the thin filament towards the centre of the sarcomere 3. Myosin detaches new ATP binds to myosin head myosin detaches from actin myosin is still in low energy state 4. Cocking of Myosin Head ATP is split by ATPase enzyme on myosin head…split into ADP and P the energy is released to put the myosin head into the high energy state back to start…… myosin binds in its high energy state with ADP and P attached still ADP and P are released and the head moves and pulls the actin new ATP binds and myosin detaches in its low energy state ATP is split to provide energy for the next powerstroke and head is cocked Muscle Contraction part II muscle cells respond all or none each cell contracts fully but since a muscle is made of tons of cells the whole muscle contraction can vary in force and duration depends on # fibers contracting simultaneously The Motor Unit MU is the nerve-muscle functional unit MU is a motor neuron and all the muscle fibers it innervates motor nerve is made of tons….hundreds of neurons neuron axons enter the muscle and branch and form NMJs with muscle fibers motor neuron will fire and all the muscle fibers it innervates will contract a MU may have 4-100 or more muscle fibers in the MU small MU = 4 muscle fibers served by one neuron…fine motor control…fingers, eyes large MU = 100 – less precise movements fibers of a MU are not clustered, they are spread through the muscle……stim of a MU causes weak contraction of entire muscle Muscle Twitch twitch = response of a motor unit to a single action potential contraction response …..contract fast then relax 3 phases 1. Latent few msec following stim ECC is occurring….AP along sarcolemma, Ttubule, calcium release, troponin…XBs starting to move muscle tension increasing but no response on myogram 2. Contraction XBs active if tension is great enough to overcome the load, the muscle will shorten 3. Relaxation calcium reuptake into SR muscle no longer contracting some twitch responses are fast and brief – eye muscles some are slow and contract longer – soleus, gastros diffs reflect metabolic properties and enzyme diffs Graded Response of Muscle Twitch muscles do not normally twitch….see in lab and in some neuromusc probs contractions are smooth and vary in strength as diff demands are placed on them graded muscle response = the variations in contraction strength to ensure proper control of muscle movement ex. allows the same muscles to …..pick up baby, crush pop can…..diff amt of strength needed for different activity can be graded by: changing frequency of stimulation changing strength of stimulus (#MUs activated) Changing Stimulation Frequency increase firing rate = increase muscular force a second electrical stimulation delivered very soon after first…rides on shoulders of first twitch…………wave summation second contraction occurs before muscle has completely relaxed more calcium is being released from SR while some is still present from the last contraction not yet reuptaken so more Ca is floating..… tension produced in second contraction produces more shortening than the first …….contractions are summed absolute refractory period is always honored if stim faster and faster…less relaxation time between twitches…….Ca concentration in sarcoplasm increases more and more and summation is greater and greater………..eventually max tension reached, no relaxation between twitches ……smooth contraction…..tetanus Stronger Stimuli recruitment controls force of contraction multiple motor unit summation activating a large number of MUs = increase in muscular force size principle…..small muscle fibers are controlled by small highly excitable motor neurons……activated first as contractile strength increases….recruit larger MUs containing larger muscle fibers….large neurons are less excitable…higher threshold, recruited later size principle allows force increases to occur in small steps all MUs can be activated at same time but usually not Muscle Tone skel muscles almost always are slightly contracted----muscle tone due to stretch receptors that are always sensitive to even small amounts of stretch in monitoring posture tone keeps muscles firm and ready to respond to stimulation…ie. primed and ready to go tone stabilizes joints and maintains posture Muscle Tension – the force generated by a contracting muscle on an object Muscle Contraction – activation of myosin cross bridges Isotonic Contraction - same/constant tension once sufficient tension has been generated to move a load the tension generally remains constant muscle will change length to move the load concentric – shortens to do work eccentric – generates force while lengthening 50% more forceful than CON more DOMS stretching during the contraction causes microtears ex. squat – bend….quads are stretching and contracting to control the movement (muscle braking) and prevent joint injury stand back up…concentric contract quads as they shorten and knees extend ECC contraction can be intentional for strengthening..pilates curl back…or ECC can be seen in the controlling part of a CON mvmt. ECC is stronger..you can curl in a bicep curl…when that is too heavy to CON contract you will still be able to ECC contract to put it down Isometric contraction – same length muscle attempts to move a load greater than the force/tension the muscle is able to develop maintenance of posture is isometric or holding joints stable while movement occurs at other muscles…ex.sit up……..neck muscle are working to hold neck stable ex. in squat….pause in bent position…..quads contracting isometrically to hold knees stable…their tension will exceed the load and then the contraction in CON so squat……ECC…ISO…CON at same time …..ISO of lumbar muscles isotonic…..thin filaments are sliding isometric…XBs are generating force but are not moving the thin filaments “spinning their wheels on the same actin binding sites” Factors affecting Muscle Contraction 1. Recruitment 2. Hypertrophy 3. Series Elastic Components 4. Degree of Muscle Stretch 1. Recruitment more motor units recruited = greater force generated 2. Hypertrophy size of muscle fiber bulkier fiber = more tension developed = more strength larger muscles have larger muscle cells with more myofibrils with more actin and myosin 3. Elastic Elements series elastic components are non-contractile components of muscle….fascia XBs initially pull the fascia taut (internal tension) and no actual muscle movement is seen once that is taut it pulls through to the ends of the muscle/bone and causes movement (external tension) time is required to take up this slack and stretch that fascia when a muscle is stimulated rapidly the series elastic component is already taken up so there is no time needed for that 4. Degree of Muscle Stretch muscle has an optimal resting length…length at which muscle can generate maximum force ideal length-tension relationship --- ideal length where the optimal amt of tension can be developed ideal – muscle is slightly stretched and thick and thin overlap optimally – permits sliding along nearly the whole filament if too stretched – no overlap…myosin heads can not attach to myosin too much overlap – sarcomere is cramped, think filaments touch and interfere with one another, no further shortening can occur optimal length – 80%-120% of resting length joint structure usually prevents movement outside this range Factors Affecting Velocity and Duration of Contraction 1. Load placed on the muscle 2. Muscle Fiber Type 1. Load - resistance heavier load = slower contraction (slower velocity) heavier load = fatigue faster heavier load = shorter duration of contraction (shorter duration) lighter load = faster contraction (faster velocity) lighter load = longer to fatigue lighter load = longer duration of contraction possible (longer duration) larger load longer latent period latent period is when that AP is traveling through Ttubules to myofibrils….when motor units are being activated…if the load is heavier, more MUs are trying to be activated slower contraction (slower velocity) shorter duration of contraction (shorter duration) too large load muscle cant move the load – isometric velocity = zero 2. Fiber Type different fiber types increase or decrease velocity of contraction different fiber types increase or decrease duration of contraction Fibers are classified based on: Speed of Contraction ATP formation pathway 1. Speed of contraction slow – slow splitting ATPase on the myosin and slower pattern of electrical activity of their motor neuron fast – fast splitting ATPase on the myosin and slower pattern of electrical activity of their motor neuron fast medium slow 2. ATP formation pathway oxidative fibers – use aerobic pathways glycolytic fibers – use anaerobic pathways slow oxidative fast oxidative fast glycolytic Fast Glycolytic fast ATPase quick neuron stimulus-response use anaerobic glycolysis few mitochondria – not needed since don’t use O2 to make ATP few capillaries – don’t need to exchange as much O2 low myoglobin – don’t need to store as much O2 high glycogen storage – use glycogen for fuel quick to fatigue – produce lactic acid and run out of ATP since produce only small amounts, run out of glycogen reserves large fibers - don’t depend on continuous nutrient and O2 diffusion from blood so the cell can be larger generate lots of power – due to large size and therefore lots of myofibrils/filaments good for : short term, rapid, intense movments Slow Oxidative slow ATPase slow neuron-stimulus response uses aerobic respiration many mitochondria – for ATP production in krebs and ETC lots of capillaries – need O2 to make ATP lots of myoglobin – need O2 to make ATP low glycogen storage – does not use it for ATP fatigue-resistant – don’t produce lactic acid, don’t run out of ATP fast small fibers – must be small to be in close contact with capillaries generate little power – due to small size, fewer fibrils and filaments good for : endurance Fast Oxidative Fibers intermediate fibers mixture of features of FG and SO fast ATPase uses aerobic respiration many mitochondria lots of capillaries high myoglobin intermediate levels of stored glycogen moderately fatigue-resistant intermediate size most muscles are made of a mixture of all types….allows muscles to have a range of contractile speeds genetically determined can alter with type of training…..strength vs endurance training Muscular Physiology IV Muscle Metabolism ATP used for: XB movement…..ATPase breaks ATP to ADP and P and releases energy stored in the bonds…this puts myosin head into high energy state ready to pivot myosin head detachment – when ATP binds myosin head detaches calcium pump – active pump for Ca back into SR ATP limited stores enough for 4-6 seconds must be regenerated fast ATP is formed by: 1. interaction ADP with creatine phosphate 2. from stored glycogen via glycolysis 3. aerobic respiration 1. Phosphorylation of ADP by creatine phosphate CP is a high energy molecule stored in muscle CP transfers its P to ADP to make ATP and creatine occurs fast while other ATP pathways are firing up very quick and efficient catalyzed by creatine kinase stored ATP and CP provide 10-15 sec of max muscle power 2. Glycolysis use glucose from blood or use glycogen stores from muscle glycolysis----2 pyruvic acid made…..2 ATP made if O2 present….pyruvic acid enter mitochondria…..krebs….ETC if O2 absent …heavy fast contraction..muscles bulge and compress blood vessels PA makes LA LA enters blood goes to liver, heart, kidney….used as energy source liver cells can change it to glucose or PA to be used again to make ATP Aerobic makes less ATP than the aerobic path makes ATP faster than aerobic path good for 30-40 sec of strenuous activity CP and anaerobic provide ATP for about 1 min of strenuous muscle activity but lots of glucose used to make small amount of ATP lots of LA produced….fatigue during rest and light-mod activity in mitoch uses O2 energy is released and transferred and captured in ATP bonds initially glycogen and glucose are used for the first 30 min then fatty acids are used 36/38ATP are made per glucose but its slow Energy Systems used during activity if enough O2 present…ATP made aerobically…..light –mod activity can continue for several hours if demands on muscle increase….need ATP faster….glycolysis begins to contribute aerobic endurance – length of time a muscle can continue to contract using aerobic pathways anaerobic threshold – point where anaerobic metab kicks in weight lifting, diving, sprinting…surge of power for few sec…ATP and CP tennis, soccer, 100 meter swim…….glycolysis marathon…aerobic Muscle Fatigue physiological inability to contract…muscle may still be receiving stimuli psychological fatigue….muscles can still contract but we feel tired prob with ECC coupling lack of ATP does not cause fatigue….lack of ATP causes contractures/rigor mortis lactic acid accumulates, alters contractile proteins..causes that ache and burn feeling….but has more effect on central/psychological fatigue…does not physiologically limit….body regulates the H well during AP transmission, K+ is lost from muscle cells…disturbs membrane potential…alters calcium release from SR P accumulates when CP and ATP breakdown…P interferes with calcium release basically short duration intense activity……ionic disturbances alter EC coupling long duration low intensity exercise…damages SR..interferes with Ca release Oxygen Debt exercise causes: lactic acid accumulation….must be converted to pyruvic acid glycogen depletion….must be replenished ATP depleted…..stores must be replaced CP depleted…..stores must be replaces all of these require oxygen…..does not happen in anaerobic exercise so these activities are deferred until O2 available….O2 debt is incurred oxygen debt = the extra amount of oxygen the body must take in for the restorative processes repay debt…….by heavy breathing lactic acid accumulates in blood…the H will leave the lactic acid enters blood high H in blood…..low pH high CO2 in blood triggers heavy breathing….. try to eliminate CO2 which frees up HCO3 so the H can bind to it to form carbonic acid… a weak safe acid used as an intermediate molecule controlling respiration Muscle Pathologies Myasthenia Gravis autoimmune….immune system attacks own body antibodies attack Ach receptors at NMJ signal not transmitted muscle weakness, paralysis, death possible Muscular Dystrophy affected muscles initially enlarge due to fat and CT deposit but muscle fibers atrophy and degenerate Duchenne MD X linked recessive….females carry it, usually affects boys muscles weaken….limbs first then progresses upwards death in 20s…respiratory failure muscle fibers lack dystrophin….strengthening protein that stabilizes the sarcolemma….therefore the sarcolemma tears during contraction..excess calcium enters cell…upsets homeostasis…damages actin and myosin and inflammatory cells accumulate in surrounding CT……the regenerative capacity of the muscle is lost….damages cells die…loss of muscle mass Smooth Muscle found in walls of hollow organs and blood vessels fibers: spindle shape small single nucleus gap junctions – specialixed groups of cells that connect adjacent cells to the AP from cell to cell arranged in sheets transmit layers: longitudinal layer – fibers run parallel to long axis of organ….contraction of these causes organ to dilate and shorten circular layer – fibers run around the circumference of the organ…contraction of this layer constricts the lumen and elongates the organ alternating contraction and relaxation of these layers mixes substances in lumen and squeezes contents through organ’s internal pathway…peristalsis functions: 1. moves substances…blood, peristalsis 2. expels contents….bile from gallbladder, urine from bladder 3. guards entrances and exits Structure: 1. no NMJ – NT releases from bulbous swellings on ends of ANS motor fibers into a wide synaptic cleft area 2. no T tubules – sarcolemma has different pouchlike infoldings (caveolae) of ECF and Ca 3. Ca enters from ECF through sarcolemma wall of inpouching Organization: 1. nonstriated, no sarcomeres 2. thick filaments are different – longer 3. filaments arranged in bundles, not sarcomeres 4. more actin per myosin 5. myosin heads along whole length..more XBs 6. powerful contractions 7. have tpopomyosin, no troponin 8. no z discs…have dense bodies…collections of cytoskeleton protein that anchor the cells..sliding of filaments pulls on this network contraction…areas of sarcolemma between the dense bodies network bulge…looks puffy RECALL…..FROM SEMESTER 1…. Glycolysis – use glucose to make pyruvic acid to fuel krebs cycle from 1 molecule of glucose: 2 ATP used 4 ATP made 2 NADH2 carrying H to be used later in ETC to make ATP 2 pyruvic acid ****result is 2 ATP and 2 NADH2 which will produce 6 ATP Pyruvic acid if no O2 present: Lactic Acid formed when the NADH gives off the H… the H joins the pyruvate to make lactic acid… the NADH2 needs to dump off the H and return to NAD to be used in glycolysis so glycolysis can continue if O2 present……pyruvic acid..to Krebs Krebs - when O2 is present, use pyruvic acid to fuel the krebs reactions to create NADH2 and FADH2 which will ultimately make ATP one pyruvic acid enters mitochondria: 3 carbons removed……3 CO2 made (1 before and 2 during krebs) 1 FADH2 created in Krebs 4 NADH2 created (1 before and 3 in krebs) 1 ATP created recall one glucose makes 2 pyruvic acid so 6 CO2 2 FADH2 8 NADH2 2 ATP ****result is 2ATP, 2 FADH2 which will produce 4 ATP, 8 NADH2 which will produce 24 ATP ETC – oxidize NADH2 and FADH2 (remove the H) so that glycolysis and krebs can continue…(glycolysis and krebs can only continue if NAD and FAD are available to pick up more H)…and so electrons transferred in the process can be captured by ATP synthase to make ATP each NADH2 that transfers H2 to the ETC contributes enough energy to make 3 ATP each FADH2 starts a little farther along so contributes less energy so 2 ATP are made SO…… glycolysis – 1 molecule of glucose 2 ATP made (4 made, 2 used) 2 NADH2 2 pyruvic acid krebs – 2 pyruvic acid 6 CO2 2 FADH2 8 NADH2 2 ATP ETC 2 NADH from glycolysis = 6 ATP 8 NADH from Krebs = 24 ATP 2 FADH from Krebs = 4 ATP end result…. 1 glucose molecule turns into CO2 and H2O and 38** ATP are created glycolysis ETC 2 ATP ……………………………….…………………………….….…2 2 NADH ……………………………..…6 ATP**……………….. 6 total ATP krebs 2 ATP ……………………………….…………………………………..2 8 NADH………………………………………24 ATP……………..…24 2 FADH……………………………………….4 ATP ………………….4 total = 38 ATP ** but the 2NADH made during glycolysis cannot enter the mitochondria easily….uses 2 ATP for transport so only 2 ATP are created from each NADH so 4 instead of 6……so 38 minus 2 = 36 Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means "grave muscle weakness." With current therapies, however, most cases of myasthenia gravis are not as "grave" as the name implies. In fact, for the majority of individuals with myasthenia gravis, life expectancy is not lessened by the disorder. The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected. What causes myasthenia gravis? Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction - the place where nerve cells connect with the muscles they control. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. Acetylcholine travels through the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction. In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. These antibodies are produced by the body's own immune system. Thus, myasthenia gravis is an autoimmune disease because the immune system - which normally protects the body from foreign organisms mistakenly attacks itself. What are the symptoms of myasthenia gravis? Although myasthenia gravis may affect any voluntary muscle, muscles that control eye and eyelid movement, facial expression, and swallowing are most frequently affected. The onset of the disorder may be sudden. Symptoms often are not immediately recognized as myasthenia gravis. In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in myasthenia gravis varies greatly among patients, ranging from a localized form, limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles sometimes including those that control breathing - are affected. Symptoms, which vary in type and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision (diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, difficulty in swallowing and shortness of breath, and impaired speech (dysarthria). The Brain basic divisions: 1. cerebral hemispheres - cortex, white matter, basal nuclei 2. diencephalon - thalamus, hypothalamus, epithalamus 3. brain stem - midbrain, pons and medulla 4. cerebellum Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei Cerebral Cortex awareness, communication, memory, voluntary movements Primary (somatic) motor cortex control voluntary movements Premotor Cortex controls learned motor skills of a repetitive or patterned nature ex. playing instrument Broca’s area motor speech area – directs muscles involved in speech production Frontal eye field controls voluntary movements of eyes Primary somatosensory cortex receive info from somatic sensory receptors, proprioceptors Somatosensory association cortex integrate sensory inputs from primary sensory cortex, to produce an understanding of what the stimulus is – size, texture, etc. Visual Areas primary visual cortex - info from retina visual association areas - uses past visual experience to interpret visual stimuli allowing recognition and appreciation of what is being seen Auditory Areas primary auditory cortex - info from hearing receptors in ear, interpret pitch loudness, location auditory association areas - perception of sound that we hear Olfactory Cortex info from receptors in superior nasal cavities conscious awareness of odors Gustatory Cortex perception of taste stimuli Visceral Sensory Area conscious perception of visceral sensations – upset stomach, full bladder Vestibular cortex conscious awareness of balance Multimodal Association areas areas that receive inputs from senses and send outputs to many areas gives meaning to info received stores info in memory, ties it to previous experience and knowledge relays info to premotor cortex, which communicates with primary motor cortex 3 major association areas Anterior Association area intellect, complex learning (cognition), personality, judgment, reasoning Posterior Association area recognizing patterns, faces, localize surroundings, bind different sensory inputs into a whole Limbic Association area emotional impact lateralization = unique abilities specific to each hemi not shared by the other cerebral dominance = the hemisphere that is dominant for language….90% of people it is the left…right handed Cerebral White Matter communication between cerebral areas and between cortex and lower CNS areas commissures – connect corresponding gray areas of the 2 hemis corpus callosum – largest commissure association fibers – connect diff parts of same hemi projection fibers – travel vertically from to or from cortex internal capsule – band formed by projection fibers at top of brain stem corona radiata – fanning/radiating of tracts above the capsule Basal Nuclei caudate nucleus putamen globus pallidus receive input from cerebral cortex and other subcortical nuclei some role in motor control, attention, cognition starting, stopping, monitoring intensity of movement inhibit unnecessary movements, help perform several actions at once as a group also called corpus striatum because the fibers of internal capsule pass by them and make it look striped Diencephalon – Thalamus, Hypothalamus, Epithalamus Thalamus afferent impulses from all senses synapse here sensory information is edited here crude recognition of sensation occurs here ie. pleasant or unpleasant. Hypothalamus contains many nuclei for visceral control and homeostasis homeostatic roles: 1. Autonomic control centre - BP, HR, digestive motility, pupil size 2. Emotional response - perceives pleasure, fear, rage, acts through ANS 3. Body temperature regulation - receives input from thermoreceptors 4. Regulation of food intake - responds to blood levels of nutrients 5. Regulation of water balance and thirst - osmoreceptors 6. Regulation of sleep/wake cycles - suprechiasmatic nucleus 7. Control endocrine system functioning - releasing hormones Epithalamus contains pineal gland – secretes melatonin – sleep inducing signal Brain Stem – Mibdrain, Pons, Medulla produce programmed automatic survival behaviours Midbrain cerebral peduncles – corticospinal/pyramidal tracts cerebellar peduncles – tracts connecting midbrain to cerebellum superior colliculi – visual reflex centres inferior colliculi – auditory relay to cortex and auditory reflex red nucleus – red…blood, iron…relay neclei in some descending motor paths that effect limb flexion (rubrospinal) Pons conduction tracts between cord and cortex and cerebellum and cortex Medulla inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum cochlear nuclei – auditory relay vestibular nuclei – vestibular (equilibrium) relay nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending somatic sensory info heading to somatosensory cortex visceral motor nuclei: cardiovascular centre - cardiac centre (HR), vasomotor (BP) respiratory centre - control rate and depth of breathing other centres - hiccupping, swallowing, coughing, sneezing hypothalamus controls visceral functions by relaying its instructions through medullary centres which carry them out Cerebellum processes inputs from cerebral motor cortex, brain stem nuclei, sensory receptors to provide precise timing and appropriate patterns of skeletal muscle contraction for smooth coordinated movements subconscious equilibrium inputs here to adjust posture and maintain balance motor cortex via relay nuclei in stem notify cerebellum of intent to initiate voluntary muscle contraction Functional Brain Systems Limbic System septal nuclei, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus, amygdale, hypothalamus, anterior thalamic nuclei emotional brain communicates with cerebral cortex creating relationship between feelings (limbic) and thoughts (cortex) Reticular Formation govern brain arousal reticular activating system – a group of neurons that send continuous impulses to cortex…keeps cortex alert ascending sensory tracts synapse with RAS which enhances their arousing effect on the cortex sensory inputs are filtered here reticulospinal tracts control skeletal muscle and some visceral motor functions The Brain 1. Cerebral Hemispheres a. Cerebral Cortex Motor Areas: Primary (somatic) motor cortex Premotor Cortex Broca’s area Frontal eye field Sensory Areas: Primary somatosensory cortex Somatosensory association cortex Visual Areas primary visual cortex visual association areas Auditory Areas primary auditory cortex auditory association areas Olfactory Cortex Gustatory Cortex Visceral Sensory Area Vestibular cortex Multimodal Association areas Anterior Association area Posterior Association area Limbic Association area b. Cerebral White Matter c. Basal Nuclei 2. Diencephalon Thalamus. Hypothalamus Epithalamus 3. Brain Stem Midbrain Pons Medulla 4. Cerebellum 5. Functional Brain Systems Limbic System Reticular Formation The Brain Cerebral Hemispheres – Cerebral Cortex, White Matter, Basal Nuclei 1. Cerebral Cortex awareness, communication, memory, voluntary movements Primary (somatic) motor cortex - control voluntary movements Premotor Cortex - controls learned motor skills of a repetitive or patterned nature Broca’s area - motor speech area – directs muscles involved in speech production Primary somatosensory cortex - receives info from somatic sensory receptors, proprioceptors Somatosensory association cortex - produces an understanding of what the stimulus is Visual Areas primary visual cortex - info from retina visual association areas - uses past visual experience to interpret visual stimuli allowing recognition and appreciation of what is being seen Auditory Areas primary auditory cortex - info from hearing receptors in ear - pitch loudness, location auditory association areas - perception of sound that we hear Olfactory Cortex info from receptors in superior nasal cavities, conscious awareness of odors Gustatory Cortex perception of taste stimuli Visceral Sensory Area conscious perception of visceral sensations – upset stomach, full bladder Anterior Association area / Prefrontal Cortex intellect, complex learning (cognition), personality, judgment, reasoning Posterior Association area / Gnostic Area interprets all sensory info of a particular situation, generates understanding of the situation, sends info to prefrontal cortex Lauguage Area / Wernickes Area interpretation of speech Visceral Association perception of visceral stimuli 2. Cerebral White Matter communication between cerebral areas and between cortex and lower CNS areas 3. Basal Nuclei caudate nucleus, putamen, globus pallidus role in motor control, starting, stopping, monitoring intensity of movement inhibit unnecessary movements Diencephalon – Thalamus, Hypothalamus, Epithalamus Thalamus afferent impulses from all senses synapse here, sensory information is edited here Hypothalamus contains many nuclei for visceral control and homeostasis 1. Autonomic control centre - BP, HR, digestive motility, pupil size 2. Emotional response - perceives pleasure, fear, rage, acts through ANS 3. Body temperature regulation - receives input from thermoreceptors 4. Regulation of food intake - responds to blood levels of nutrients 5. Regulation of water balance and thirst - osmoreceptors 6. Regulation of sleep/wake cycles - suprechiasmatic nucleus 7. Control endocrine system functioning - releasing hormones Epithalamus contains pineal gland – secretes melatonin – sleep inducing signal Brain Stem – Mibdrain, Pons, Medulla produce programmed automatic survival behaviours Midbrain cerebral peduncles – corticospinal/pyramidal tracts cerebellar peduncles – tracts connecting midbrain to cerebellum superior colliculi – visual reflex centres inferior colliculi – auditory relay to cortex and auditory reflex red nucleus – red…blood, iron…relay neclei in some descending motor paths that effect limb flexion (rubrospinal) Pons conduction tracts between cord and cortex and cerebellum and cortex Medulla inferior olivary nuclei – relay info on muscles and joint stretch to cerebellum cochlear nuclei – auditory relay vestibular nuclei – vestibular (equilibrium) relay nucleus gracilis and nucleus cuneatus – sensory relay nuclei for ascending somatic sensory info heading to somatosensory cortex visceral motor nuclei: cardiovascular centre - cardiac centre (HR), vasomotor (BP) respiratory centre - control rate and depth of breathing other centres - hiccupping, swallowing, coughing, sneezing hypothalamus controls visceral functions by relaying its instructions through medullary centres which carry them out Cerebellum provides precise timing and appropriate patterns of skeletal muscle contraction for smooth coordinated movements, subconscious Functional Brain Systems Limbic System emotional brain, communicates with cerebral cortex creating relationship between feelings (limbic) and thoughts (cortex) Reticular Formation govern brain arousal, keeps cortex alert