Conductive tissue/NMJ Junction Flashcards by John Rose

Give 2 examples of location for electrical synapse

cardiac and some types of smooth muscle

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are “many to one” synapses common?

yes

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EPSPs do what to a post synaptic cell?

i. Name examples of neurotransmitters

Depolarize and bring closer to threshold potential
i. purines, acetylcholine (ACh), norepinephrine,
epinephrine, dopamine, glutamate, aspartate

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IPSPs do what to a post synaptic cell?

i. Name examples of neurotransmitters

Hyperpolarize and bring further from threshold potential

ii. γ-aminobutyric acid (GABA), glycine, serotonin, and nitric oxide

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overlapping of multiple presynaptic inputs in rapid succession from THE SAME presynaptic neuron is an example of …..

temporal summation

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multiple presynaptic inputs arriving simultaneously is an example of …..

spatial summation

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name location of a presynaptic input that would have the largest effect on whether or not an AP is fired in the POSTsynaptic cell.

received by a dendrite near the axon hillock

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main mechanism for synaptic fatigue

ready neurotransmitter supply is exhausted

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list steps of neurotransmitter transmission to NMJ from
(first step) AP in neuron → depolarize presynaptic terminal

….

(last step) Choline taken up by presynaptic terminal via Na+/choline cotransporter

AP in neuron depolarize presynaptic terminal
Calcium channels in presynaptic terminal open
Calcium causes vesicles to fuse with presynaptic membrane and release ACH into synaptic cleft
ACH binds motor end plate where there is nicotinic receptor that opens cation channel
Na flows in; K flows out. Cell gets depolarized to EPP (-50 mV)
EPP spreads and causes AP generation in muscle fibers
ACH broken down by ACH esterase
Choline taken up by presynaptic terminal via Na+/choline contransporter

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Where do EPP and AP occur respectively?

EPP–motor end plate

AP-muscle fibers (not end plate)

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what is a quantum and how is it related to mini EPP?

quantum is amount of neurotransmitter in one vesicle. it depolarizes end plate in a quantal fashion, so one vesicle contents equate to a mini epp.

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MOA of botulinum

i. <3 word clinical finding after botulinum toxicity

blocks release of ACH from presynaptic cell (blocks vesicle fusion)
i. flaccid paralysis

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MOA of curare

i. what does it do to EPSP?

competes with ACH for nicotinic receptors

i. decreases size of EPSP

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uses of curare

skeletal muscle relaxation during anesthesia

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uses of botox

upper motor neuron disorders
chewing swallowing disorders
hair loss
muscle spasms
excessive sweating

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MOA of ach esterase inhibitors

prevent degradation of ach in synaptic cleft

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uses of ach esterase inhibitors

myasthenia gravis, alzheimers, parkinsons

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where is the dihydropyridine (dhp) receptor located?

dhp receptor is located on the t-tubule and is sensitive to voltage

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where is the ryanodine receptor located?

ryanodine receptor is on the terminal cisternae of SR

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how do the dhp and ryanodine receptor interact

dhp and ryanodine are touching. dhp receptor is responsive to voltage from AP. dhp then conformational changes and activates ryanodine receptor which lets calcium out of SR

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explain calcium binding to …. protein in short filament complex

calcium binds to troponin c, cooperatively. causes tropomyosin to move and reveal binding sites for myosin.

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is serca active constitutively yes or no?

yes

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recocking of the myosin head is initiated by what

hydrolysis of atp to adp and pi

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what causes conformational change resulting in decreased affinity of myosin for actin?

atp binding to myosin

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what causes power stroke?

pi release

what is tetanus?

sustained muscle contraction due to temporal summation of APs

does smooth muscle have troponin?

no so always free binding sites

sources of Ca+ for skeletal and smooth muscles

skeletal: only from SR smooth: from SR (IP3) and voltage+ ligand Ca+ channels on PM (sarcolemmel membrane)

effect of calcium concentration on skeletal and smooth muscles

skeletal muscle: all or nothing | smooth: calcium gradient

regulation of calcium in skeletal and smooth muscle

Skeletal: SERCA: removes calcium from skeletal muscle causing relaxation Smooth: lowering calcium or activating myosin phosphotase which inhibits myosin atpase activity

describe calmodulin and MLCK interaction

in smooth muscle, ca binds calmodulin. this activates mlck. mlck then phosphorylates myosin head, greatly increasing its atpase activity (myosin is always high atpase activity for skeletal)

how can calcium be lowered in smooth muscle? | 4 ways

1. Hyperpolarization closes voltage-gated Ca channels 2. Direct inhibition of Ca channels by ligands like cAMP and cGMP 3. Inhibition of IP3 production 4. Increase in Ca/ATPase activity

local anesthetics block ....

Sodium channels

potency of local anesthetics is directly proportional to

lipid solubility (e.g not good if acidosis which charges basic part of drug)

what functional group class is: procaine?

ester

what functional group class is: tetracaine?

ester

what functional group class is: lidocaine?

amide

what functional group class is: mepivacaine

amide

what functional group class is: bupivacaine

amide

best drug for old ppl with heart issues | i. why

mepivacaine (carbocain) | i. no coadmin of epi needed

local anesthetic fxn group class metabolized by liver

amide

local anesthetic fxn group class metabolized in serum quickly

ester

which is more sensitive to anesthetics? large or small nerve fibers?

small fibers more sensitive bc have no or less myelination

rank nerve classes in terms of sensitivity from LEAST to most sensitive.

A-alpha, A-beta, A-gamma, A-delta, B, C.

C type neurons are

nociceptor and sympathetic efferents

alpha type neurons are

motor

list 2 disadvantages to epi coadmin

ischemia | cardiovasc effects

list two systems in body affected by LA spillage into circulation

CV (arrythmia) and CNS (initially depression then excitation/seizure)

selectivity of ion channels (list 2 things)

charge and size of pore

conductance of ion synonym

permeability

typical resting potential of a cell is

-75mV

equilibrium potential for an ion is

potential at which ion flow is in equilibrium across a membrane (balanced with concentration gradient flow)

Sort Na+ Ca+ K+ and Cl- as higher concentration in cell or outside cell

Na--outside cell higher Ca--outside cell higher K--inside cell higher Cl--outside cell higher

what is a way you could change the resting membrane potential of a cell in lab?

changing extracellular potassium concentration, since the cell is most permeable to potassium

what pump maintains membrane potential?

Na/K atp pump

at rest, which conductance is higher, Na or K?

what is lvl for threshold potential usually

-55mV

all or none principle of APs

All AP’s of a cell will cause the same voltage changes.

describe permeability changes of Na and K ions during phases of excitation

see doc

basis for absolute refractory period

closure of sodium inactivation gates in RESPONSE to depolarization

basis for relative refractory period

higher potassium conductance (mostly hyperpolarization) | Na channels are closed but available

Accomodation

slow depolarization closes inactivation gates (bc it is slow allows the gates to close before an AP can ever be fire), even tho activation gate is open the inactivation one is closed.

internal diameter is ..... proportional to rate of conduction and .... to internal resistance

directly....inversely

membrane resistance is .... proportional to conduction velocity

directly

capacitance is .... proportional to conduction velocity | more myelin causes ..... capacitance

inversly | less

C and IV neuron types

slow pain

Rank the following nerve classes as fastest, medium, or slowest: Ia, Ib, A alpha A beta, A gamma, A delta, B, C.

Fastest: A alpha, Ia, Ib Slowest: C

name two nerve fiber types/classes that are not myelinated

C and IV