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Chapter 16 Neural Integration II: The Autonomic Nervous System and Higher-Order Functions Sensory Motor General (15) Somatic (15) Special (17) Autonomic (16) fig. 15-1 fig. 16-1 Autonomic Nervous System (ANS) regulate homeostasis works independent of consciousness Autonomic Nervous System (ANS) compared to Somatic NS fig. 16-2 fig. 16-3 Sympathetic prepare body for heightened levels of somatic activity “fight or flight” response •increased mental alertness •increase metabolic rate •reduced digestive/urinary fn •activation of energy reserves •increase respiration rate •increase heart rate, bp •activation of sweat glands fig. 16-7 parasympathetic stimulates visceral activity “rest and repose” conserve energy promote sedentary activities •decrease metabolic rate •decrease heart rate, bp •increase secretion-digestion •more blood to digestive system •stimulate urination/defecation sympathetic parasympathetic ENS enteric nervous system complex visceral reflexes sympathetic nervous system preganglionic neurons T1 to L2 lateral horn of spinal cord lots of divergence (1 to many) project to ganglia (3) sympathetic chain ganglia collateral ganglia adrenal medulla fig. 16-4 fig. 16-5 sympathetic nervous system collateral ganglia celiac stomach, liver, gall bladder pancreas and spleen superior mesenteric small intestine proximal 2/3’s of large intestine inferior mesenteric large intestine, kidneys, bladder reproductive organs fig. 16-4b Adrenal medulla receives preganglionic sympathetic input synapse on neuroendocrine cells of medulla cells secrete E or NE into blood epinephrine norepinephrine adrenaline noradrenaline fig. 16-4c CRISIS sympathetic activation controlled by centers in the hypothalamus increased alertness RAS feelings of energy and euphoria (disregard for danger, insensitivity to pain) Increase heart and lung activity (controlled by pons and medulla) Elevation of muscle tone Mobilization of energy reserves sympathetic neurotransmitters preganglionic neurons use ACh (cholinergic) postganglionic neurons release NE (adrenergic) postganglionic cells have varicosities instead of axon terminals fig. 16-6 sympathetic neurotransmitters affect is longer lasting than at a neuromuscular jn (Ach; 20 msec) NE affects its targets until it is reabsorbed or broken down (seconds) NE adrenal medulla lasts even longer (minutes) sympathetic neurotransmitters Most of the NE released is reabsorbed by the neruon (50-80%) reabsorbed NE is re-used or broken down by MAO (monoamine oxidase) the rest diffuses away and is broken down by COMT in the tissues sympathetic neurotransmitters receptors for NE Two classes alpha beta both are G-proteins (second messengers; 12) neurotransmitters and neuromodulators How do they work? 1. direct effect on membrane potential 2. indirect effect on membrane potential 3. diffusion into cell 2. fig 12-17 fig. 12-17 sympathetic neurotransmitters alpha receptors a-1 more common release intracellular Ca2+ stimulates target cell a -2 lowers cAMP levels in cell (inhibitory on target cell) found on parasympathetic cells sympathetic neurotransmitters beta receptors in membranes of many organs heart, lungs, liver, muscle, … changes metabolic activity of target cells (intracellular cAMP) sympathetic neurotransmitters beta receptors b-1 increased metabolic activity skeletal muscle cardiac output b -2 inhibitory relax smooth m. in resp. tract easier to breath (asthma) sympathetic neurotransmitters beta receptors b-3 found in adipose tissue causes lipolysis release fatty acids for metabolism sympathetic neurotransmitters other transmitters ACh sweat glands in skin (secretion) blood vessels to brain and muscle (dilation of vessels) NO (nitric oxide) vasodilation in brain and muscle to here 3/16/07 lec# 27 sympathetic summary uses sympathetic chain collateral ganglia adrenal medulla short preganglionic, long postgang. excessive divergence (2 doz +) pregang. cells release ACh Most postgang. cells release NE a few use ACh, NO Response depends on receptors (a,b) sympathetic summary neurotransmitters and receptors: pre- ACh post- NE a receptors a most commonstimulatory ACh b a b inhibitory b increase inhibitory skel. muscle (airways) cardiac output b fat cells lipolysis NO Parasympathetic nervous system fig. 16-7 Parasympathetic nervous system preganglionic cells in nuclei in: midbrain pons medulla oblongata spinal cord travel with: CN III, VII, IX, X pelvic nerves S2 to S4 Parasympathetic nervous system preganglionic cells: less divergence than sym. (6-8) postganglionic cells: in terminal ganglia (near organ) or intramural (in organ) effects more localized and specific CN III VII IX X pelvic fig. 16-8 Parasympathetic nervous system CN III, VII, IX control visceral structures in the head CN X neck, thoracic and abdominal cavities (75% of parasympathetics) Parasympathetic activation constrict pupils close vision stimulate digestion secretions secretion of hormones-cellular nutrient use sexual arousal changes increase smooth m. activity - digestive sys. stimulate/coordinate defecation contract urinary bladder for urination constrict airways reduce heart activity Parasympathetic neurotransmitters ACh fast acting inactivated quickly by AChE localized effects Parasympathetic neurotransmitters Receptors two types: nicotinic on ganglion cells most muscles (SNS) lead to epsp muscarinic parasym. muscle, glands G proteins epsp or ipsp longer lasting Parasympathetic neurotransmitters Receptors nicotinic nicotine poisoning (50 mg): vomiting, diarrhea, high bp rapid heart rate, sweating,… muscarinic nausea, vomitting, diarrhea, constriction of airways, low bp low heart rate 100 keys (pg. 530) “The preganglionic neurons of the autonomic nervous system release acetylcholine (ACh) as a neurotransmitter. The ganglionic neurons of the sympathetic division primarily release norepinephrine as a neurotransmitter (and both NE and E as hormones at the adrenal medulla). The ganglionic neurons of the parasympathetic division release ACh as a neurotransmitter. Table 16-2 fig. 16-9 summary and interactions sympathetic widespread distribution parasympathetic visceral structures served by CN or in abdominopelvic cavity most organs receive input from both (dual innervation) actions are usually opposite anatomy of dual innervation head parasympathetics with CN sympathetic via superior cevical ganglion thorax and abdomen sympathetics and parasympathetics mix autonomic plexuses cardiac pulmonary esophageal celiac hypogastric fig. 16-10 autonomic tone background stimulation allows for more control two examples: autonomic tone 1. heart receives dual innervation review: cardiac muscle has pacemaker ACh from parasym. slows rate NE from sympath. accelerates rate both are released all the time but, normally parasym is in control can modulate heart rate up or down autonomic tone 2. blood vessel diameter review: only get sympathetic background NE from sympathetic partial constriction of vessels need more blood stop NE release increase ACh release blood vessels dilate autonomic tone 2. blood vessel diameter review: only get sympathetic background NE from sympathetic partial constriction of vessels need less blood increase NE release blood vessels constrict autonomic integration and control centers are found all over the CNS primary motor cortex (UMN) … …LMN of cranial and spinal reflexes also visceral reflexes example visceral reflexes shine a light in one eye… …both pupils will constrict (consensual light reflex) parasympathetic in the dark… …pupils dilate (pupillary reflex) sympathetic visceral reflexes motor muclei controlling the pupils are controlled by hypothalamic centers responding to emotions too nauseated/queasy sexually aroused pupils constrict pupils dilate autonomic integration and control visceral reflex arc receptor (sensory neuron) processing center (interneurons) two visceral motor neurons long or short reflexes autonomic integration and control long reflexes equivalent to the spinal reflex (13) processing (interneurons) in CNS fig. 16-11 autonomic integration and control short reflexes bypass the CNS processing (interneurons) in ganglion fig. 16-11 autonomic integration and control short reflexes bypass the CNS processing (interneurons) in ganglion used extensively in digestive system ENS autonomic integration and control other autonomous reflexes respiration, cardiovascular, … table 16-4 autonomic integration and control other autonomous reflexes respiration, cardiovascular, … parasympathetic sympathetic divergance organ or organ system activated as a whole higher levels of control centers for: cardiovascular respiratory swallowing salivation digestive secretions peristalsis urinary functions nuclei in medulla oblongata hypothalamus integration of ANS and SNS see fig. 16-12 Higher order functions •need cerebral cortex •involve conscious and unconscious •not part of “hardwiring” subject to modification and adjustment memory / learning consciousness sleep / arousal brain chemistry / behavior aging Higher order functions memory / learning fact memories bit of info skill memories learned actions short term (primary) memory consolidation long term secondary may fade with time tertiary lifetime fig. 16-13 Higher order functions memory / learning memory consolidation involves amygdoloid body hippocampus damage hippocampus cannot convert short-term to long-term existing long term remains intact Higher order functions memory / learning memory consolidation involves amygdoloid body hippocampus nucleus basalis ? damage to nucleus leads changes with Alzheimers (later) Higher order functions memory / learning memory consolidation long term memories stored the cerebral cortex association areas some memories are dependent on the activity of a single neuron to here 3/19 Lec #28 Higher order functions memory / learning memory consolidation anatomical/physiological D neurons and synapses Higher order functions memory / learning memory consolidation increased nt release facilitation at synapses additional synaptic connections create anatomical changes in circuits 1 circuit/1 memory = memory engram Higher order functions memory / learning memory consolidation take time nature intensity frequency influenced by: of stimulus strength, extremeness, frequency, drugs Higher order functions memory / learning memory consolidation hippocampus NMDA-receptors chemically gated Ca2+ channels blocking NMDA receptors prevents formation of long-term memory Higher order functions memory / learning amnesia loss of memory because of disease or trauma Higher order functions memory / learning amnesia retrograde lose memory of past events e.g., head injury-forget accident anterograde inability to store new memories common sign of senility living in “new” surroundings Higher order functions memory / learning amnesia can occur suddenly or progresively recovery can be: complete partial non-existent depending on problem Higher order functions memory / learning amnesia diazepam (valium) Halcion can cause brief periods of anterograde amnesia 100 Keys (pg. 539) “Memory storage involves anatomical as well as physiological changes in neurons. The hippocampus is involved in the conversion of temporary, short-term memories into durable long-term memories.” Higher order functions States of consciousness conscious unconscious awake coma really asleep asleep… Higher order functions sleep deep sleep aka., slow wave sleep non-REM sleep REM sleep rapid eye movement sleep Higher order functions sleep deep sleep body relaxes cerebral activity is minimal heart, resp, bp, energy utilization all decrease (30%) Higher order functions sleep REM sleep active dreaming D resp. rate, bp EEG looks similar to awake, but less response to outside stimuli decrease in muscle tone (intense SNS inhibition) eye muscles escape inhibition Higher order functions sleep REM sleep cycles of REM, non-REM fig. 16-14a fig. 16-14b Higher order functions sleep sleep disorders 25% of Americans abnormal REM sleepwalking … Higher order functions arousal awakening controlled by the reticular formation extensive interconnections with: sensory motor integrative nuclei Higher order functions arousal RAS reticular activating system from medulla to midbrain projects to thalamus cortex activity of cortex is proportional activity of RAS fig. 16-15 Higher order functions arousal RAS sleep is ended by activation effects last short time (min) positive feedback keeps us awake Higher order functions arousal nuclei maintains alertness NE + RAS serotonin promotes sleep nuclei 100 keys (pg. 541) “An individual’s state of consciousness is variable and complex, rangeing from energized and “hyper” to unconscious and comatose. During deep sleep, all metabolic functions are significantly reduced; during TEM sleep, muscular activities ar inhibited while cerebral activity is similar to that seen in awake individuals. Sleep disorders result in abnormal reaction times, mood swings and behaviors. Awakening occurs when the reticular activating system becomes active; the greater the level of activity, the more alert the individual.” Brain chemistry and behavior changes in the balance of nt’s can affect brain function. sleep-wake cycles Huntington’s disease Brain chemistry and behavior Huntington’s disease destruction of ACh and GABA secreting neurons in the basal nuclei loss of basal nuclei, frontal lobes loss of muscle control and intellectual abilities Brain chemistry and behavior serotonin LSD activates serotonin receptors hallucinations enhance serotonin activity Brain chemistry and behavior serotonin block serotonin depression and anxiety slow serotonin removal increase serotonin (SSRI’s) Prozac, Paxil, Zoloft Brain chemistry and behavior serotonin variety of pathways delivering serotonin to nuclei and higher centers affect sensory interpretation and emotional states Brain chemistry and behavior dopamine needed to reduce muscle tone stimulated by “speed” causes “schizophrenia” disturbances in mood thought and behavior Aging affects all body systems (including brain) changes begin around 30 reduction in brain size and weight (cortex) reduction in # of neurons (cortex) decreased blood flow to brain (arteriosclerosis) changes in synaptic organization (fewer) cellular changes accumulations inside the cells (tangles) accumulations outside the cells (plaques) Aging Alzheimer’s progressive disorder characterized by loss of higher order cerebral functions 15% of people over 65 50% of people over 85 100,000 deaths/year Aging Alzheimer’s areas develop “plaques” and “tangles” ?? genetics late onset chromosome 19 early onset chromosomes 21 and 14 no cure, but may slow progression Integration of Nervous System with other body systems monitors all systems adjusts their activity level of impact is variable skeletal muscle cardiac muscle fig. 16-16