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UNIT 2- Review Sheets Pathology Studied Multiple sclerosis (MS) Ptosis Myasthenia Gravis An immune-mediated inflammatory demyelinating disease of the central nervous system. Without the myelination and because of the scarring where the myelin sheath was, the neuron is not as likely to conduct the action potential. Refers to the droopiness of the eye often seen in myasthenia gravis patients. An autoimmune disorder where antibodies attack ACh receptors, which can cause flaccid paralysis if left untreated. Ptosis of the eyelids is a sign of this disorder. Caused by denervation/neuropathy; sedentary life style; plaster cast; space flight (zero gravity) Muscle performance: degeneration of contractile proteins; decreased maximum force of contraction and velocity of contraction Fiber loss can occur if disuse of muscle for 1-2 years; very difficult to replace lost fibers Atrophy This condition is opposite to hypertrophy (normal way to increase muscle mass) Caused by near maximal force development (e.g., weight lifting) Increases in actin and myosin Myofibrils split FUNCTIONAL CLASSIFICATION OF NEUROTRANSMITTER RECEPTORS TYPE Example Where found? Channel within receptor? Second messenger? ionotropic nAChR metabotropic mAChR Skeletal muscle Postganglionic neuron of ANS Involuntary effectors of parasympathetic nervous system Some on skeletal muscle Found also on erector pili, sweat glands, and blood vessels to the skin Yes Yes NO NO NO Yes! G protein activated Effector protein: phospholipase C Second messengers: DAG, IP3, Ca+ Late effector protein: Protein kinase C Effect: protein activity changes: e.g., ion channel permeability changes NO Yes! G protein activated Effector protein: adenylyl cyclase Second messenger: cAMP Late effector protein: Protein kinase A Effect: protein activity changes: e.g., ion channel permeability changes α (1) and β(1,2,3) Involuntary effectors of sympathetic nervous system Nervous System Chart AUTONOMIC NERVOUS SYSTEM- two neuron chain to involuntary effectors (cardiac muscle, smooth muscle, glands) What Location of the Preganglionic neuron Parasympathetic Nervous System (craniosacral) T1-L2 in the intermediolateral cell column (IMLCC) of the spinal cord Terminal ganglia- these are found in the walls of the involuntary effectors. Sympathetic ganglia of the sympathetic trunk Collateral ganglia on the inferior mesenteric, superior mesenteric and the celiac trunk. Long Short Short Long ACh ACh Cholinergic receptors nACh receptors ACh Cholinergic receptors nACh receptors ACh if on the body wall with muscarinic receptors on sweat glands, erector pili muscle, and blood vessels to the skin Nepi and epi if the body Adrenergic ALWAYS FOUND IN THE CNS! Brain-CN#3,7,9,10 S2-S4 in the sacral lateral gray column (SLGC) the spinal cord Location of the Postganglionic neuron ALWAYS FOUND OUTSIDE THE CNS! That means they are found in the PNS in autonomic ganglia. Length of the Preganglionic Fiber Length of the Postganglionic Fiber Neurotransmitter used by preganglionic cell Receptor type on Postganglionic neuron Neurotransmitter used by Postganglionic neuron Sympathetic Nervous System (thoracolumbar) Receptors found on effectors Muscarnic receptors Preganglionic Fiber Postganglionic Fiber Cholinergic Cholinergic Adrenergic receptors (Alphas and Betas) sometimes: mACHr (see notes above for muscarinic explanation). Cholinergic Adrenergic/ sometimes Cholinergic SOMATIC MOTOR NERVOUS SYSTEM-one neuron to effector (voluntary- skeletal muscle) Cell body found where? Ventral Gray horn of spinal cord or brain nuclei for cranial nerves 3, 4, 5, 6, 7, 9, 10, 11, 12) Neurotransmitter/ Receptor used ACh Primarily nAChR but some mAChR are found, too Effects Skeletal muscle contraction SPECIFIC EFFECTS IN ORGANS INNERVATED BY THE AUTONOMIC NERVOUS SYSTEM ORGAN Sympathetic Effects Eye: Iris smooth muscle, ciliary muscle Dilation of pupil (contraction of radial fibers of ciliary muscle) Lacrimal Gland Vasoconstriction Salivary Gland Scant secretion Heart Lungs-Bronchi Increased rate and force of contraction Dilation of airways Blood Vessels Vasoconstriction Gut Decreased peristalsis and secretion Bladder Inhibition of urine Penis Ejaculation Adrenal Medulla Secretion of epinephrine into bloodstream Skin-outer areas of the body including head, neck and extremities; pilo erector muscles and sweat glands Vasoconstriction, sweat, erection of pilo erector muscles Receptor Neurotransmitter Alpha Adrenergic-Nor Epinephrine Alpha Adrenergic-Nor Epinephrine Alpha Adrenergic-Nor Epinephrine Beta 1-Adernergic –Nor epinephrine Beta 2-Adernergic Nor epinephrine Alpha Adrenergic-Nor Epinephrine Adrenergic Nor epinephrine Parasympathetic Constriction of pupil (contraction of sphincter like muscles) Ciliary muscle contracts for accommodation Secretion Receptor Neurotransmitter Muscarinic Metabotropic- Ach Increased gut motility and secretion Muscarinic Metabotropic- Ach Muscarinic Metabotropic- Ach Muscarinic Metabotropic- Ach Muscarinic Metabotropic -Ach Muscarinic Metabotropic- Ach Muscarinic Metabotropic -Ach Adrenergic Nor epinephrine Bladder contraction and release Muscarinic Metabotropic- Ach Adrenergic Nor epinephrine Modified “postganglionic” cell Erection Muscarinic Metabotropic- Ach Copious Secretions Slowed Rate Vasoconstriction Vasodilatation None Muscarinic Metabotropic -ACh ANS Stimulants Type Drug / Toxin Phenylephrine – stimulates alpha receptors (this is in Sudafed PE) Sympathetic nervous Isoproterenol – stimulates beta1 and beta2 receptors system gains more Albuterol – stimulates beta2 receptors control over the Ephedrine – increases release of norepinephrine effector Amphetamine – increases release of norepinephrine Parasympathomimetics Nicotine – stimulates nACh receptors Muscarine – stimulates mACh receptors (causes profuse Parasympathetic sweating, gut motility (diarrhea), salivation, pupillary nervous system gains constriction) more control over the Pilocarpine – stimulates mACh receptors (causes profuse effector sweating, gut motility (diarrhea), salivation, pupillary constriction) Sympathomimetics Effect o Stimulates or mimics the effects of adrenergic receptors; some increase the release of these neurotransmitters o Sympathetic system gains more control o Stimulates receptors/ mimics the binding of ACh on all kinds of ACh receptors o Parasympathetic system gains more control Blockers / Inhibitors Type Monoamine Oxidase Inhibitor (MAOI) Drug / Toxin Anti-depressant (no particular brands were given) Effect o Inhibits MAO from degrading catecholamines in the synapse Selective Serotonin Reuptake Inhibitor (SSRI) Prozac Ecstasy o Inhibits reuptake of serotonin into the presynaptic membrane o Leads to potentiated effects of serotonin (lasts longer) Na+ VGC Blocker Lidocaine - used as anesthesia (dentist shoots this into trigeminal nerve) Tetrodotoxin (TTX) – from liver of puffer fish and newts Saxitoxin (STX) – dinoflagellates accumulate in shellfish during red tides Clostridum botulinum “Botox” Undercooked turkey Dented food cans Atropine o Flaccid paralysis o Inhibits depolarization Vesicle Blocker mAChR Blocker (blocks parasympathetic nervous system— sympathetic nervous system would gain more control!) nAChR Blocker K+ VGC Blocker Curare – made from tree sap; large dose can cause asphyxiation Tetraethylammonium (TEA) AChE Blocker (reversible) Neostigmine – typically given to a person with Myasthenia Gravis Physostigmine – typically given to a person with Myasthenia Gravis AChE Blocker (irreversible) Diisopropylfluorophosphates (DFP) Sarin (must ventilate until reproduction of more AChE occurs through gene expression!) Inhibitory NT release Blocker Tetanus exotoxin Black widow venom Adrenergic Blocker (sympathetic blocker) Phentolamine is an alpha receptor blocker Propranolol is a beta1 and beta2 receptor blocker Allows parasympathetic nervous system to gain more control! o Flaccid paralysis o Inhibits neurotransmitter release by blocking the ability for vesicles to dock to synaptic membrane o Flaccid paralysis o Inhibits muscarinic receptors – a few found on voluntary effector (skeletal muscle) but mainly found on the involuntary effectors used by the parasympathetic nervous system: smooth muscles (intestines/eye), heart, and glands (pancreas/ salivary glands). Also sympathetic uses this receptor for sweat glands/erector pili muscle and blood vessels to the skin. o Would increase heart rate, bronchiole dilation, dry skin (why?), dry mouth, constipation, pupillary dilation o Flaccid paralysis o Inhibits nicotinic receptors (mainly skeletal muscles) o Spastic paralysis o Inhibits repolarization o Spastic paralysis o Temporarily inhibits AChE from degrading ACh in the synapse; therefore ACh effects are potentiated (that means they last longer). Skeletal muscle contraction more likely to occur/lasts longer. o NOTE: these drugs also potentiate the effects of ACh used by the ANS (postganglionics stimulated) and by effectors of the parasympathetic system. o Spastic paralysis o Permanently inhibits AChE from degrading ACh in the synapse o NOTE: this drugs also potentiates the effects of ACh used by the ANS (postganglionics stimulated) and by effectors of the parasympathetic system. o Spastic paralysis o Blocks the release of inhibitory neurotransmitters (e.g., GABA, Gly), from the presynaptic neuron, therefore the post-synaptic neuron is more likely to be excited from EPSPs that continue to arrive (spatial summation) thus making the neuron closer to threshold and more likely to fire an action potential. For a somatic motor neuron, this means the skeletal muscle it innervates will also be receiving more end plate potentials and thus contracting more. o Reduces the effectiveness of the sympathetic nervous system on these receptors and lets parasympathetic NS gain more control of body/effector o Blocked alpha receptors (found on eye and blood vessels) would lead to pupillary constriction (parasympathetic effects are still fine) and vasodilation. o Blocked B1 and B2 through propanolol leads to decreased heart rate and bronchiole constriction (drug is contraindicated for asthmatics!) because parasympathetic effects are in more control. Name NEUROTRANSMITTERS Receptors Important notes Acetylcholine nAChR (iontropic) mAChR (metabotropic- uses IP3/DAG/Ca+2) Glutamate GluR GABA-major inhibitory neurotransmitter GABA receptor Glycine Gly R Norepi/epi alpha 1 (eye and most blood vessels) Beta (1 and 2; heart and lung, respectively) Beta 3- found on adipose tissue These receptors are metabotropic and would use the cAMP pathway Serotonin serotonin receptors this neurotransmitter is excitatory for nAChR neurotransmitter may be inhibitory for mAChR (e.g., parasympathetic innervation to the heart causes hyperpolarization of specialized cells’ prepotential) Nearly all excitatory neurons found in CNS use it—e.g., it causes EPSP (increases sodium permeability) and is used to stimulate somatic motor neurons in spinal cord. Antagonists to Glutamate receptor help stop neuronal death after stroke- block receptor Too much glutamate leads to excitotoxicity in postsynaptic neuron due to unregulated calcium influx Too little leads to psychosis Inhibitory neurotransmitter: would cause IPSP on postsynaptic neuron by increasing permeability to K+ or Cl-. For example, would cause an IPSP in a somatic motor neuron in the spinal cord. Too little GABA leads to excitability of postsynaptic neuron (seizures/convulsions) Anticonvulsants are drugs that are “GABA-like” (agonists) and lead to inhibition of postsynaptic neuron (IPSP) Valium- increases release of GABA and leads to inhibition of postsynaptic neuron (IPSP) Benzodiazepines- stimulate GABA receptor (more inhibition of postsynaptic cell) Ethanol – stimulate GABA receptor (more inhibition of postsynaptic cell) Inhibitory neurotransmitter: would cause IPSP on postsynaptic neuron by increasing permeability to K+ or Cl. Stimulating these receptors would give more sympathetic responses. Inhibiting these receptors would give more parasympathetic responses. Stimulating alpha 1: vasoconstriction and pupillary dilation Stimulating B1: increased heart rate and force of contraction Stimulating B2: increased bronchiole dilation Stimulating B3: increased adipose tissue mobilization. Norepi/Epi normally diffuse out of synaptic cleft very readily, but MAO is also present to degrade neurotransmitter. MAOI potentiates norepi effects (makes last longer). Selective serotonin reuptake pumps on presynaptic membrane help remove serotonin from synaptic cleft. SSRI’- selective serotonin reuptake inhibitors are antidepressant drugs-potentiates the effects of serotonin Ecstasy drug inhibits SSR, too!