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23 Cards in this Set
- Front
- Back
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Resting membrane potential(RPM)
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electrical diff b/t inside & outside of cell
-70mV for a typical neuron +65 for Na+ -85 for K+ b/c it's close to norm K is more permeableto cell than Na 2 forces that determine it: chemical & electrical |
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Different channels
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-non gated (leak)Na & K
-gated (ligand)&(voltage) -mechanically gated (thermal) |
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neural siganling
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2 types: AP & Graded
AP: -active -only occur along axon -always & only depolarizing -all or none -any given AP's are idendtical -initiated @ axon hilock Graded potentials: -occur anywhere -depolerize & hyperpolerize -initiated @ synapse -decay w/ distance -variable amplitude -travel short distances |
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Graded potentials
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result from sensory & interneuron inputs
-no direct release of NT's have 2 catagories: EPSP (postsynaptic potential)-excititory (depol) IPSP-inhibitory(hyperpol) -the potentials are dependant on length & time, charge decreases w/distance (length) capacitence & resistance make up the time factor and cause a delay in charge reaching it's max voltage |
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Threshold potential
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voltage it takes to get Na gates to open & start AP happens 15mV above -73
-sub threshold: no AP -supra:always AP |
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2 ch. that elicit charges from AP's
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Na:
has 2 gates acitve gate: is closed @ rest,open in open state, & open in inactive state inactive gate: open in rest state,open in open state, closed in inactive state inhibited by lidocaine,fugu toxin,scorpion toxin K: has 1 gate stays open until repol (-50mV) |
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3 phases of AP's
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depol-
sum of GP's pass axon hillock,Na ch. open & let Na in, cell gets +, ends when Na ch are inactive repol- K ch open K goes out cell starts to go back to RPM hyperpol- K gates close slowly @ RPM if neurons don't hyperpol there's a shorter refractory period which causes hyperexcitability which causes siezures from lots of AP's |
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Frequency of AP
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-is limited by refractory period
refractory period: absolute-period where another AP can't be generated no matter how large the stim. relative: lasts until after hyper phase, if a EPSP is strong enough then an AP can be generated again |
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Conduction
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dependant on 2 things:
diameter- if it's inc you have dec cytop resistance inc length=rapid reflex myeination: -inc length constant by dec leakage of signals - dec time -less ion diffusion |
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Sympathetic neurons
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-cell bodies(originate)are in spinal cord(T1-L3)
-preganglionic neurons are short and post are long -synapse @ sympathetic chain ganglia or form splachnic nerves and synapse @ prevertebral region -preganglionic axons are myelinated -pregang have AcH as thier NT w/ nicotinic receptors on postgang axon -postgang axons are unmyelinated (C fibers) - postgang have Norepinepherine for NT and alpha 1,beta1,beta2 receptors on effector organs |
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Parasympathetic neurons
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1.CN 3 occulomotor(midbrain)-pupil constriction,focus of lens
2.CN 7 facial-lacrimal (pons)gland,salivations 3.CN 9 glossopharyngeal(medulla)-parotid gland control 4.CN 10 vagus(medulla)- heart,lungs,gi tract -cell bodies also found in lateral horn of S2-S4:lower colon,bladder -pregang have AcH NT's and nicotinic receptors -postgang have AcH as NT and muscarinic receptors at effector organ -postgang organs are short and axons are unmyelenated |
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Organs that receive only sympathetic inn.
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-most vessels
-adrenal medulla -piloerector musc. -sweat glands |
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MS
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-autoimm. disease
-demyelination anywhere in CNS -more frequent in women -pins and needles sensations in limbs(spinothalamic tract plaque) -patch of blindness in one eye (optic nerve tract plaque) -clumsiness (cerebellar plaque) -weakness in legs (corticospinal plaque) -symptoms get worse w/ a temp |
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Guilian-Barre syndrome
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-occurs after minor infectious illness
-autoimm. attacks on PNS myelin (motor neurons) -progressive weakness in an ascending pattern -resp failure |
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2 types of neurochemical communication
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1.autoreceptors-presynaptic relese of NT
2.retrograde-post synaptic NT release and presynaptic actions i.e. NO-very imp for memory formations |
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Ionotropic receptors
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-ligand gated (ch. open by hormones,2nd messengers)
-fast=rapid change in memb pot. -glutamate NT: *majority of CNS synapses have this *always excititory *overactive glut neurons cause epilepsy tx w/ phenyltoin -GABA NT: *major inhibitory NT in brain *opens Cl or K ch. *loss of inhibition causes epilepsy and loss of balance *insomnia *anxiety Glycine NT: *major inhibitory NT in spinal cord *opens Cl ch. *target of severe toxins i.e. strychnine is a competitve antagonist causes restlessness,spasms,paralysis *hyperekplexia(startle disease)exagerated reflexes |
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Metabotropic receptors
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-second mess. system
-slow transmission -modulation of synaptic fxn Neuropeptides: *released after high levels of activity(bursts of APs) these cause release of glutamate and NPs *imp for pain NPs are endorphins,enkephalins interferes w/ pthwy for sleep cntr,n/v,contipation Amine NT: *includes catecholimines (dopamine),NE,seretonin *found in brainstem *can be excititory or inhibitory *dopamine=addiction inc levels of dopamine=>schizophrenia dec levels=>parkinsons *seratonin and NE=> disorders of arousal and ADD |
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Drugs and toxins that affect neuromuscular transmission
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d-tubocurarine a musc relaxant used w/ a gen anesthetic:
-musc relaxant -binds to nicotinic AcHR -induces paralysis(resp musc) Botulinum toxin: -blocks rel of AcH from presyn terminal(vesicle fusion blkd) *descending paralysis Botox: -cervical dystonia neck contraction -blepherospasm invol eyelid closure -exessive sweating |
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Diseases of NMJ
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Myasthenia gravis:
-inc inAChR turnover -block of ACh binding -weakness and fatigueability of musc. w/ activity -affects cranial musc 1st=>facial=>ptosis eye=> diplopia is dbl vision -slurred speech Lambert-Eaton myasthenic syndrome: -autoimm. disease,abs form against presynaptic Ca ch. at NMJ -musc weakness -strength improves w/ activity -loss of reflexes -lots of pt.s have small cell CA of lung |
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Hypothalamus
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controls:
-bld osmolarity -renal clearence -drive for thirst and salt consumption regulates: -gender id and sexual orienttion -mating behaviors Coordinates response to life thretening situations: -coordinates para and symp and regional bld flow |
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Central control of motor fnxs
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-afferent neurons in drgs carry info from visceral organs to nucleus in medulla
-they're activated by pressure and stretch, changes in chem(o2)ischemia, |
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Sympathetic junxal receptors
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-all are NE:
alpha1: -post junxnal andrenoreceptors -cause cont of sm musc alpha 2: -prevent NT release beta1: -inc heart rt. -betablkers act here -renal vasoconsricters -inc contractility of heart beta 2: -pre and post -bind epineph prejunxally -promote NE release -postjux relax sm musc |
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Horners syndrome
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-loss of symp tone to hed and neck
-from interruption of hypothalamic control -degeneration of cells at T1 or T3 or peripheral damage -symptoms are: ipsilateral,no eye dilation (myosis),pupil wil retract to lite,ptosis,sunken eyeball (enophthalmos),loss of sweat glnd secretion |
