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PDBIO 305: Peripheral Nervous System - Week 5

by: Kirsten Notetaker

PDBIO 305: Peripheral Nervous System - Week 5 PDBIO305

Marketplace > Brigham Young University > Physiology and Developmental Biology > PDBIO305 > PDBIO 305 Peripheral Nervous System Week 5
Kirsten Notetaker
GPA 3.95

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These notes cover the peripheral nervous system, including both the afferent and efferent branches. Discussion of pain and pain receptors, inhibition of neurons, sympathetic vs. parasympathetic sti...
Human Physiology
David Thomson
Class Notes
Physiology, peripheral, nervous, system, neuron
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This 5 page Class Notes was uploaded by Kirsten Notetaker on Friday October 14, 2016. The Class Notes belongs to PDBIO305 at Brigham Young University taught by David Thomson in Fall 2016. Since its upload, it has received 10 views. For similar materials see Human Physiology in Physiology and Developmental Biology at Brigham Young University.

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Date Created: 10/14/16
Peripheral Nervous System (PNS) Afferent division of the PNS = sensory division Positioning of the spinal cord Dorsal and ventral roots Afferent fibers enter spinal cord via (dorsal root) Efferent fibers leave the spinal cord via (ventral root) Ganglion: collection of cell bodies (term applies outside of CNS) Sensory pathways st Stimulus -> recepndrs -> afferent (1 order) neuron -rdspinal cord or brainstem -> 2 order neuron -> thalamus -> 3 order neuron -> cortex Sensory intensity Remember – neurons either fire or they don’t, action potentials are all- nothing, NOT “big” or “small” Intense sensory activation doesn’t result in intense action potentials Instead, intensity is coded by the frequency of action potentials (frequency coding) or the number of afferent nerves activation (population coding) Frequency coding Greater stimulus (greater graded potentials) -> greater likelihood of overcoming relative refractory period & reaching threshold -> more frequent action potentials Population coding Greater stimulus -> depolarization (recruitment) of more receptors -> increased frequency on afferent neuron OR depolarization of increased number of afferent neurons -> greater frequency of action potentials arriving in CNS Sensory localization Sensory (receptive) fields overlap When stimulus hits overlapping areas, both neurons fire Lateral inhibition Interneurons at synapse between 1 & 2 st ndorder neurons inhibit nearby neurons from transmitting signals (Primary neuron sends EPSP to inhibitory interneuron, which sends IPSP to nearby neurons) Inhibit through neurotransmitters which inhibit calcium channels at synaptic terminals Neurotransmitters used are endogenous opiates, GABA, glycine This means the signal coming from the neuron doing the inhibiting will be relatively stronger arriving in the brain than the signals coming from the nearby inhibited neurons -> helps to pinpoint where stimulus is coming from Presynaptic Inhibition Neurotransmitters (glycine, GABA, etc.) inhibit calcium channels at synaptic terminals -> less calcium enters presynaptic neuron -> less neurotransmitter released -> reduced effect on postsynaptic neuron Types of receptors – mechanoreceptors, thermoreceptors, nociceptors Pain Primarily a protective mechanism meant to bring a conscious awareness that tissue damage is occurring or is about to occur Storage of painful experiences in memory helps us avoid potentially harmful events in future Receptor: nociceptor Two best known pain neurotransmitters Substance P – activates ascending pathways that transmit nociceptive signals to higher levels for further processing Glutamate – major excitatory neurotransmitter Two types of pain, conducted by different afferent fibers Fast pain – sharp, usually temporary, transmitted by fast fibers Slow pain – dull/throbbing/achy, transmitted by slow fibers (C- fibers), persists chronically Gate-control theory Slow pain inhibits inhibitory interneurons Collaterals from other sensory receptors stimulate interneurons, blocking pain transmission Endogenous Opiates Brain has built in analgesic system Suppresses transmission in pain pathways as they enter spinal cord Depends on presence of opiate receptors Endorphins, enkephalins, dynorphin Induced by exercise, stress, acupuncture Prostaglandins Prostaglandin released from damaged tissue greatly enhances receptor response to noxious stimuli Lowers nociceptor’s threshold for activation Some pain relief can be achieved by inhibiting prostaglandin production Non-opioid analgesics (i.e. aspirin) Efferent division = autonomic NS Autonomic Nervous System Autonomic nerve pathways consist of 2 neurons (remember afferent pathways have 3) Preganglionic fiber – cell bodies of preganglionic fiber lie in the spinal cord Postganglionic fiber These fibers synapse within a ganglion Ganglion = cluster of neuron cell bodies outside of CNS Effector organs = skeletal or smooth muscle, glands, adipose tissue, etc. Autonomic neurotransmitters Parasympathic system = “rest & digest” – most activity at mealtimes, during rest & sleep Neurotransmitter – ACh (acetylcholine) Sympathetic system = “fight or flight” – most activity during exercise, fear, flight or fight Neurotransmitters ACh (from preganglionic neurons) Norepinephrine (from postganglionic neurons) Epinephrine (from adrenal medulla) ACh is stimulatory (generates EPSPs) on postganglionic neurons But on target organs it can be stimulatory or inhibitory – depends on receptors Ex: decreases heart rate Autonomic receptor types Cholinergic receptors – receive ACh + Nicotinic receptor+ – open cation channels (lots of Na comes in, some K released -> depolarization -> excitation) Muscarinic receptors – initiate cell signaling cascades, several subtypes ACh binds to receptor -> G-protein subunits dissociate -> G- protein binds to K channel -> hyperpolarization -> less excitation Adrenergic receptors (for NE) Activated by epinephrine & norepinephrine 2 major classes: α and β Two subtypes of each: α1, α2 and β1, β2 Alpha 1 Alpha 2 Beta 2 Adenylate cyclase converts ATP into cAMP Acetylcholinesterase breaks down ACh into acetate & choline Choline is recycled to make more ACh Norepinephrine is recycled directly back into the releasing cell Effect of sympathetic (S) vs. parasympathetic (P) stimulation on various organs Heart: S increases HR (mainly beta-1), P decreases HR (HR = heart rate) Blood vessels: S vasoconstriction (alpha-1), P vasodilation (of penis & clitoris vessels only) Stomach, intestines: S decreases activity (alpha-1), P increases activity Lungs: S bronchioles dilate (beta-2), P bronchioles constrict Adrenal medulla: S releases epinephrine Liver: S glycogenolysis (glycogen -> glucose, alpha-1 & beta-2) Adipose tissue: S lipolysis Agonists & antagonists Sympathetic agonist = drugs that mimics effect of norepinephrine Sympathetic antagonist = drugs that block effect of norepinephrine Parasympathetic agonist = drugs that mimic effect of acetylcholine Parasympathetic antagonist = drugs that block effect of acetylcholine Voluntary vs. autonomic pathways Voluntary: motor neuron goes straight from spinal cord or brain to muscle Autonomic: preganglionic neuron goes from spinal cord or brain to ganglion, postganglionic neuron goes from ganglion to organ


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