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physiology > Synaptic Transmission and the Neuromuscular Junction > Flashcards

Synaptic Transmission and the Neuromuscular Junction Flashcards

1
Q

What is a synapse

A

a specialized gap region that permits a neuron (or

nerve cell) to pass an electrical or chemical signal to another neuron or to the target effector cell

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2
Q

What is the difference between chemical and electrical synapses

A

eletric direct electrical continuity by gap junctions.

indirect chemical neurotransmitter that diffuse to other cell.

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3
Q

what is a gap junction made of?

A

vlakke arrays of connexons, each consisting of 6 connexin monomers.

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4
Q

how do the multiple connexons physically conncted two cells.

A

via multiple aqueous channels

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5
Q

What two kind of chemical syapses are there

A

ionotropic and metabotropic

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6
Q

What is the agonist of electrical and chemical synapses?

A

electrical none

chemical e.g ACh

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7
Q

membrane proteine of electrical synapse

A

connexon

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8
Q

membrane proteine of chemical synapse

A

ionotropic, receptro/channels

metabotropic: receptro/G protein

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9
Q

delay in transmission for each type of synapse

A

electrical, instant
ionotropic 1ms
metabotropic seconds to minutes

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10
Q

What kind of nerve is the vagus nerve and what does it do?

A

parasympathetic, produces a substance (ACh) responsible for depression of the heartbeat.

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11
Q

is ACh inhibitory or excitatory?

A

both

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12
Q

what are reciprocal synapses?

A

pass electrical current with equal efficiency in both directions

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13
Q

what are rectifying synapses?

A

Allow current only in one direction.

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14
Q

how can intrinsic rectification be altered?

A

gap junctions composed heterotypic channels

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15
Q

what are heterotypic channels?

A

a gap junction that is composed of two hemichannels, each made up of a different connexin monomer.

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16
Q

are chemical synapses reciprocal or rectifying?

A

rectifying

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17
Q

are chemical channels one or unidirectional for signal propogateion adn why?

A

unidurectional, because presynaptic cell can produce retorgade sygnaling molecules and receptors on presynaptic membrane can inhibit or facilitate the realse of a transmitter.

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18
Q

How do vescular transporters concentrate neurotransmitters inside?

A

energy on an H+ electrocehmical gradient

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19
Q

what does a increase of intracellular Ca2+ do at the presynapse

A

triggers the fusion of synaptic vesicles with the presynaptic membrane

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20
Q

How is the process of chemical synapses terminated?

A

enzymatic destruction of the transmitter (e.g., hydrolysis of ACh by ace­tylcholinesterase), (b) uptake of transmitter into the presynaptic nerve terminal or into other cells by Na + -dependent transport systems, or (c) diffusion of the transmitter molecules away from the synapse.

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21
Q

what are ligands.

A

agonists

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22
Q

what is the difference between ionotropic receptors and metabotropic receptors?

A

ionotropic aganist gated ion channels.

metabotropic. receptors coupled to G protein.

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23
Q

what are the subunits of a G protein?

A

α and βγ subunits

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24
Q

what do the α and βγ subunits produced by the Activation of a metabotropic G protein–linked receptor?

A

they iniate a wide variety of cell responses by direct interaction with either ion channel proteins or other second-messenger effector proteins.

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25
Q

what is the nicotonic AchR

A

ionotropic receptor

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26
Q

what is the muscarinic AchR?

A

metabotropic recptor at the atrial parasympathetic synapse of the heart

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27
Q

what does the activation of Muscarinic receptor do

A

activates the G protein, which opens an inward rectifier K+ channel, or GIRK. which leads to hyperpolarisation which leads to inhibition of cardiac excitation.

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28
Q

what does does the activation of the nictonic receptor do?

A

opens the AChR channel resulting in increase of permabilkty of NA and K., which leads to muscle contraction.

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29
Q

what does Acetylcholinesterase do?

A

breaks down acetylcholine.

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30
Q

what is a motor unit.

A

all the muscle fibers innervated by the axon from one motor neuron

31
Q

what is the end plate?

A

neuromuscular junction

32
Q

Where is the neuromuscular junction?

A

synaptic contact with a muscle fiber.

33
Q

What are boutans

A

bulb-shaped ending that finally contact the muscle fiber.

34
Q

what do the postjunctional folds do

A

increase increase surface area of muscle plasma.

35
Q

what is the basal lamina

A

a extracellualr matrix in the synaptic cleft containing various proteins that mediate adhesion of the neuromuscular junction and play important roles in synapse development and regeneration.

36
Q

what and where is AChE and what does it do

A

acetylcholinesterase in basal lamina , hydroplyses ACh to choline and acetate.

37
Q

where are the vesicles produced

A

the cell bodies of motor neurons in the spinal cord.

38
Q

how are the vesicels translocated to the nerve terminal

A

by microtubule-mediated process of fast axonal transport

39
Q

what is choline acetyltransferase

A

enzyme that syntheses ACh from choline and acetyl outside the vesicle.

40
Q

What does the ACh-H exchanger do

A

moves ACh inward the vesicle and H+ out

41
Q

how is the process of the ACH-H exchanger driven?

A

vesicular proton electrochemical gradient (positive voltage and low pH inside), which is produced by the vacuolar-type H pump.

42
Q

is vacuolar-type H pump passive or acxtive?

A

active, uses ATP

43
Q

what are active zones

A

regions where vesicles fuse and ach is released

44
Q

where are the most AChRs at neuromuscular joints

A

at the tops of postjunctional folds.

45
Q

is the delevery of neurotransmitters to a location precise

A

yes

46
Q

what is EPP

A

end plate potential

47
Q

To what is the revarsal potential of end plate current close?

A

0mV

48
Q

to what are AChR permeable

A

NA, K and Ca, not anions

49
Q

What happens to Vm when nicotinic AChR channels open?

A

V m shifts to a value between E K (approximately −80 mV) and E Na (approximately +50 mV).

50
Q

what kind of potential is EPP

A

excitory postsynaptic potential.

51
Q

Whata re hyperpolarizing postsynaptuc responses called?

A

inhibtory postsynaptic potentials.

52
Q

serotonin and glutamate are .. selective

and glycine and GABA are … selective

A

serotonin and glutamate are cation selective

and glycine and GABA are anion selective

53
Q

what are depolarizing postsynaptic responses called

A

excitatory postsynaptic potentials.

54
Q

What is dendrotoxin

A

K+ antagonist

55
Q

what is tetanus and botulinum toxin

A

proteine toxins made by bacteria, ACh release antagonist

56
Q

what is physostigmine and DFP

A

acetylcholinesterase antagonist

57
Q

what is nicotine en acetylcholine

A

AChR channel agonist

58
Q

what is d -tubocurarine and a-Bungarotoxin

A

AChR channel antagonist

59
Q

what is tetrodotoxin, Saxitoxin and u-conotoxin

A

Muscle Na channel antagonist

60
Q

what is ω-conotoxin

A

peptide toxin, Ca2+ channel antagonist

61
Q

what is tetrodoxotin en Saxitotoxin

A

small guanidinium neurotoxins of neuronal Na+ channel antagonist

62
Q

how does dendrotoxin facilitate ACh release?

A

Because it block K+ so the memrbane cant repolarise and more Ca2+ enters the cell.

63
Q

What does tetanus do.

A

increase of muscle tension, (begint met kaak). these toxins inhibit synaptic transmission at the spinal cord, neurons that would normale inhibit muscle contraction.

64
Q

what does botulism cause

A

paralysis of skeletal muscle, and a vierty of symptoms that are related to inhibition of cholinergic nerve endings in the autonomic nervous system.

65
Q

what anatgonist is used to treath muscle spams.

A

botuliism

66
Q

what antagonist is used to threath strabismus (a condition in which both eyes cannot focus on the same object because of abnormal hyperactivity of particular eye muscles).

A

botulism

67
Q

what is botox and how long does it last

A

botulinium toxin, smooth wrinkles by local paralysis of facial muscles. to 6 months

68
Q

what are carbamycholine and succinylcholine and what is difference with normale stof

A

agonist AChR

resistent to AChE so prolonged effect.

69
Q

what molecule is used for sugery and why

A

succinycholine, to prevent excitation because of inactivation of Na channels.

70
Q

what leads to desensitization of the AChR

A

agonising, a AChR for a long time.

71
Q

how can d-Tuborcurarine be cured

A

increase in concentration of the natural agonist ACh by binding competition. which can be produced indirectly by an inhibitor of AChE such as neostigmine

72
Q

what is pancuronium

A

stronger agonist of AChR than d-tubocuraine, used for surgery.

73
Q

what is the difference between organophosphorus compounds and physostigmine/Neostigmine

A

organophosphorus is irreversible anti AChE drug

74
Q

what are anatoxin and fasciculin?

A

natural organophosphorus (inhibitor of AChE)

physiology (8 decks)

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