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23 Cards in this Set

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Resting membrane potential(RPM)
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
Different channels
-non gated (leak)Na & K
-gated (ligand)&(voltage)
-mechanically gated (thermal)
neural siganling
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
Graded potentials
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
Threshold potential
voltage it takes to get Na gates to open & start AP happens 15mV above -73
-sub threshold: no AP
-supra:always AP
2 ch. that elicit charges from AP's
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)
3 phases of AP's
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
Frequency of AP
-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
Conduction
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
Sympathetic neurons
-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
Parasympathetic neurons
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
Organs that receive only sympathetic inn.
-most vessels
-adrenal medulla
-piloerector musc.
-sweat glands
MS
-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
Guilian-Barre syndrome
-occurs after minor infectious illness
-autoimm. attacks on PNS myelin (motor neurons)
-progressive weakness in an ascending pattern
-resp failure
2 types of neurochemical communication
1.autoreceptors-presynaptic relese of NT
2.retrograde-post synaptic NT release and presynaptic actions
i.e. NO-very imp for memory formations
Ionotropic receptors
-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
Metabotropic receptors
-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
Drugs and toxins that affect neuromuscular transmission
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
Diseases of NMJ
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
Hypothalamus
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
Central control of motor fnxs
-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,
Sympathetic junxal receptors
-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
Horners syndrome
-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