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Autonomic Nervous System ANS Honors Anatomy & Physiology for copying
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Comparison Of Autonomic & Somatic Nervous Systems
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2 Neuron Chain
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Preganglionic Neurons SympatheticParasympatheitc 1st neuron in spinal cord: thoracic and lumbar spinal nerves 1st neuron in 4 cranial nerves in the brain stem (III, VII, IX, X) or in S2 –S4 of spinal cord
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Postganglionic Neurons SympatheticParasympathetic 2 nd neuron in sympathetic trunk ganglion, a chain of ganglion that is found on either side lateral to spine 2 nd neuron in individual ganglion closer to organ it serves both sympathetic & parasympathetic neurons lie outside CNS
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Axons of Autonomic Nerves Preganglionic: – in cranial or spinal n. (from CNS ganglion) – myelinated Postganglionic: – from ganglion visceral effector – unmyelinated
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ANS Neurotransmitters based on the neurotransmitter they produce & release autonomic neurons are classified as either: 1.Cholinergic release acetylcholine (ACh) 1.Adrenergic release norepinephrine (NE) aka noradrenalin
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Cholinergic Neurons & Receptors Cholinergic neurons include: 1.all Sympathetic & Parasympathetic preganglionic neurons 2.Sympathetic postganglionic neurons that innervate most sweat glands 3.all Parasympathetic postganglionic neurons
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Receptors that bind ACh called cholinergic receptors 2 types: 1.Nicotinic receptors in plasma membranes & dendrites of symp. & parasymp postganglionic neurons & in NMJ 1.Muscarinic receptors in plasma membrane of all effectors (smooth muscle, cardiac muscle, glands) Muscarine: mushroom poisonmimics actions of ACh
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ACh when activates nicotinic receptors depolarization (excitation) when activates muscarinic receptors sometimes depolarization, sometimes hyperpolarization (inhibition) depending on the cell
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NE most sympathetic postganglionic neurons are adrenergic Adrenergic receptors bind both NE & Epinephrine (Epi) 2 types receptors: 1.Alpha receptors (α) – subtypes: α1, α2 2.Beta receptors (β) – subtypes: β1, β2, β3
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αlpha & βeta Receptors α1 & β1 produce excitation when activated α2 & β2 receptors cause inhibition of effector tissues β3 found only on cells of brown adipose where activation causes thermogenesis (heat production)
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αlpha & βeta Receptors cells of most effectors have either α or β receptors some visceral effectors contain both NE stimulates α more strongly than β Epi is potent stimulator of both
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MAO MonoAmine Oxidase: inactivates NE in synaptic cleft group of pharmaceuticals that are MAO inhibitors so prolong effect of NE
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Agonists substance that binds to & activates a receptor in the process mimicking the effect of a natural neurotransmitter or hormone example: phenylephrine is an adrenergic agonist @ α1 receptors; used in cold remedies – constricts blood vessels in nasal mucosa reduces production of mucus
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Antagonists substance that blocks receptors so prevents the natural neurotransmitter or hormone from exerting its effect example: propanolol a β1 blocker, used to treat HTN decreases heart rate & force of contraction lowers BP – side effects: hypoglycemia, mild bronchoconstriction, decreases frequency & severity of migraines
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Autonomic Tone balance between sympathetic & parasympathetic activity regulated by hypothalamus – if turns up sympathetic tone, turns down parasympathetic tone @ same time
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Sympathetic Responses dominate during physical or emotional stress occur during “E situations” – Exercise – Emotions – Emergency – Excitement
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Sympathetic Responses Fight or Flight Response – pupils dilate – HR, force of contraction, & BP increase – airways dilate – vessels to kidneys & GI tract constrict slowing down digestion & urine production – vessels muscles (skeletal & cardiac), liver, & adipose tissue dilate – hepatocytes increase glycogenolysis & adipose increase lipolysis blood glucose increases – anything nonessential slowed down
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Sympathetic Stimulation effects longer lasting than parasympathetic responses (NE lasts longer in synaptic cleft than ACh) effects are more widespread (more tissues activated)
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Parasympathetic Responses enhance “rest & digest” activities remeber SLUDD: – Salivation – Lacrimation – Urination – Digestion – Defecation
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Disorders of the ANS Raynaud’s phenomena: digits become ischemic after exposure to cold or w/ emotional stress due to excessive sympathetic stimulation of smooth muscle in arterioles in digits & increased response to stimuli that cause vasoconstriction
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Raynaud’s Phenomenon treatment options: Ca++ channel blockers to relax smooth muscle Prazosin: blocks α receptors which blocks smooth muscle contractions
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