0209101030 0211100830 - Mfm Ii - Neuromuscular Junction (Fitzovich)

Front 1

What are neuroneuronal and neuroeffector synapses?

Back 1

neuroneuronal - neuron to neuron synapse
neuroeffector - neuron to affected cell

Front 2

What type of junction allows for electrical transmission because of its very low electrical resistance?

Back 2

gap junctions

Front 3

What is unique about electric synapses that does not exist in chemical synapses?

Back 3

electrical synapses can propagate signals bidirectionally, but "rectification" is present, which means that there is a directional preference. there is also a trivial synaptic delay with an electrical synapse.

Front 4

What two ions, when stored in high concentrations in the cell can disrupt an electrical synapse?

Back 4

Ca
H

Front 5

Where are voltage gated channels found?

Back 5

Outside of the synaptic cleft

Front 6

Where are ligand gated channels found?

Back 6

in the synaptic cleft on the affected cell.

Front 7

Where are Ca++ channels found?

Back 7

on the synaptic bulb of the effector nerve cell. Ca++ will rush into the synaptic bulb when an AP reaches the bulb. this causes exocytosis of vesicles containing acetylcholine which interacts with the affected cell's cholinergic nicotinic receptors. this binding causes ligand-operated channels to increase gNa and gK which causes a transient depolarization called an EPP.

Front 8

What receptor type receives acetylcholine at the neuro-muscular junction?

Back 8

cholinergic nicotinic receptors!

Front 9

What is an EPP?

Back 9

endplate potential that is caused by transient depolarization as a result of simultaneous gNa and gK at the subsynaptic muscular cell membrane. The EPP very quickly resolves because acetylcholine caused it, and it's quickly hydrolyzed by acetylcholinesterase and that closes off the Na/K channels.

Front 10

Can the EPP cause an action potential?

Back 10

not on it's own. the EPP activates voltage-gated receptors on any place that is no subsynaptic on the cell membrane. that propagates the AP... the voltage-operated Na/K channels.

Front 11

What electrical phenomenon occurs with an EPP that does NOT happen with an AP? It depends on time and distance.

Back 11

attenuation (here called decrement)

Front 12

What does the synthesis and subsequently availability of acetylcholine depend on?

Back 12

acetyl CoA inside the cell will combine with choline that is endocytised. choline gets in against its concentration gradient by using the EC Na gradient. Na and choline both must bind to a peptide that allows them both in simultaneously. Thanks, Na!

Front 13

Aside from the postjunctional neuromuscular junction, what other types of postjunctional scenarios have nicotinic receptors and what are their exclusive action?

Back 13

autonomic ganglia, CNS

nicotinic receptors always cause depolarization by simultaneously increasing gNa and gK

Front 14

What is the acetylcholine receptor?

Back 14

cholinergic nicotinic receptor

Front 15

What is a motor unit?

Back 15

alpha motor neuron from the CNS that interfaces with several muscle spindles at the neuromuscular junction. neuron, junction and muscle spindle necessary for a complete innervation and action

Front 16

What happens when acetylcholinesterase is blocked?

Back 16

at first there will be spastic paralysis and eventually flaccid paralysis because acetylcholine cannot be cleared from the acetylcholine receptor

Front 17

What types of receptors are muscarinic and nicotinic?

Back 17

BOTH are cholinergic

Front 18

What is an alpha toxin like curare and cobra venom?

Back 18

competitive antagonists at nicotinic receptors that prevents acetylcholine and cause flaccid paralysis

Front 19

What is succinylcholine?

Back 19

partial agonist binding to nicotinic receptors which produces a long lasting receptor activation because it's not degraded by cholinesterase. this causes a depolarization conduction block -> spastic paralysis and eventually flaccid paralysis

Front 20

Why don't curare, cobra venom, and succinylcholine work at other places besides the nueromuscular junction?

Back 20

they are too polar to penetrate the ANS

Front 21

What nicotinic antagonists can penetrate the ganglia?

Back 21

ganglionic blockers such as mecamylamine, hexamethonium

Front 22

What causes myasthenia gravis?

Back 22

AChR antibodies are formed that bind to and inhibit or destroy nicotinic receptors

Front 23

What does botulin/botulinum/botox do?

Back 23

inhibits ACh release, so if you inject ACh, the receptor will react. good differentiator

Front 24

What is alpha-latrotoxin?

Back 24

black widow spider venom that stimulates ACh release -> spasm

Front 25

What are muscarinic receptors?

Back 25

cholinergic receptors found in ANS junction in cardiac muscle, smooth muscle, glands, CNS.

Front 26

What is the significant of M types in regard to muscarinic receptors?

Back 26

two types of muscarinic receptors
M1 - second most common type of cholinergic receptors (1st being nicotinic) in ANS ganglia that cause slow depolarization by \/ gK
M2 - cause relaxation of smooth muscle and cardiac muscle by hyperpolarization by /\ gK, \/ gCa
M3 - /\ intracellular free Ca++ to contract smooth muscle; release NO of endothelial cells causing relaxation of smooth muscle
M4 - /\ gK, \/ gCa of CNS
M5 - /\ intracellular Ca++ in CNS

Front 27

So what is acetylcholine? An excitatory or inhibitory neurotransmitter?

Back 27

BOTH! because the action doesn't depend on the neurotransmitter. it depends on the receptor
cholinergic nicotinic = excitatory
cholinergic muscarinic M1 = excitatory
cholinergic muscarinic M2 = inhibitory

Front 28

In general what do muscarinic receptors do to cardiac, smooth, and skeletal muscles?

Back 28

cardiac - decreases force
smooth - increases force
skeletal - nothing, they aren't there, only nicotinic

Front 29

What is the significance of atropine and scopolamine?

Back 29

both are muscarinic receptor blocks

Front 30

What is a drug that can be used as long as it is a very QUICK application in order to reverse irreversible acetylcholinesterase inhibition?

Back 30

pralidoxime

Front 31

What is the difference between neuromuscular junction, neuronal synapse, and CNS synapses?

Back 31

they can be one-to-one relation, one-to-many relation, or many-to-one relation depending on what is required to bring a cell to threshold and what interfaces in the synapse

Front 32

What are EPSPs and IPSPs?

Back 32

excitatory postsynaptic potentials
inhibitory postsynaptic potentials

Front 33

How are EPSPs accomplished in nicotinic receptors?

Back 33

simultaneous gNa and gK increase

Ca and Mg involvement occurs in other types of receptors

Front 34

How are IPSPs accomplished in nicotinic receptors?

Back 34

/\ gCl and maybe/sometimes /\ gK