Synaptic Physiology I Flashcards Preview

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Flashcards in Synaptic Physiology I Deck (77):
1

The summation of excitatory and inhibitory potentials in neurons is called _____.

synaptic integration

2

What is facilitation?

residual Ca++ builds up inside the nerve terminal from previous APs to allow increased strength of new APs

3

This is the spontaneous exocytosis of a single synaptic vesicle.

MEPP (Miniature End Plate Potentials)

4

What is the strength of the NMJ synapse?

strong

5

Drugs like amphetamine, cocaine, and Prozac exert their actions by _____ of monamine transmitters like dopamine and serotonin.

blocking reuptake

6

What is synaptic depression?

depletion of releasable synaptic vesicles, reducing the strength of new APs

7

What would happen without the sodium channels at the NMJ?

total paralysis bc the depolarization wouldn't spread

8

What is synaptic integration?

the summation of excitatory and inhibitory potentials in neurons

9

What is exocytosis?

the process of vesicle and surface membrane lipid fusion to create a pore by which the NT can diffuse out of the cell

10

What does MEPP stand for and what does it mean?

Miniature End Plate Potentials; the spontaneous exocytosis of a single synaptic vesicle

11

Name 2 kinds of diseases that weaken the NMJ synapse.

  • those that reduce the amount of NT secreted
  • those that block ACh receptor

12

Drugs like ____, ____, and ____ exert their actions by blocking reuptake of monamine transmitters like dopamine and serotonin.

amphetamine, cocaine, and Prozac

13

What is the speed of the NMJ synapse?

fast

14

Drugs like amphetamine, cocaine, and Prozac exert their actions by blocking reuptake of monamine transmitters like ____ and _____.

dopamine and serotonin

15

In the CNS the major excitatory NT is ____.

glutamate

16

What is the "intelligence" of the CNS?

smart

17

What is the effect of the NMJ synapse?

excitatory

18

Slow synaptic transmission is called _____.

neuromodulation

19

Name 2 types of Ca++ pumps in the plasma membrane.

  1. primary active transporter
  2. Na+/Ca++ exchanger (antiporter)

20

How long does synaptic vesicle recycling take?

a few seconds in a well-rested synapse; a few minutes in a hard working one

21

This is the process of vesicle and surface membrane lipid fusing to create a pore by which the NT can diffuse out of the cell.

exocytosis

22

Motor neurons in the spinal cord send myelinated axons through _____ and _____ to connect with skeletal muscle fibers.

ventral roots; peripheral nerves

23

Virtually every psych drug in use today work specifically at _____.

synapses

24

_____ selectively blocks inhibitory synaptic transmission to produce a powerful, persistent, involuntary skeletal muscle contraction.

Tetanus toxin

25

The main channel opened by glutamate is _____.

an NSC channel

26

What is the "intelligence" of the NMJ?

stupid

27

This is the product of the stimulation of the excitatory input that causes depolarization.

excitatory post-synaptic potential (EPSP)

28

A decrease in K+ ion permeability of the post-synaptic membrane = ______.

depolarization

29

What is the resting membrane potential of a muscle fiber?

-80mV

30

What is the threshold for an AP in a muscle cell?

-50mV

31

What is the motor end plate?

the end of the motor axon where it loses its myelin sheath and splays onto the muscle fiber

32

What is myasthenia gravis?

  • an autoimmune disease
  • Abs to ACh receptors
  • results in profound weakness upon exertion

33

What is the NT for the CNS synapse?

  • ACh
  • glutamate
  • GABA
  • 5-HC
  • dopamine
  • aspartate
  • glycine
  • ATP
  • histamine
  • NE

34

Ca++ ions that flowed into the motor nerve terminal will be _____.

pumped out of the cell

35

These are small protuberances from dendrites that make synaptic contact with incoming axon terminals.

dendritic spines

36

What is the NT for the NMJ synapse?

ACh

37

Where does AChE come from?

the synaptic cleft

38

A single motor axon innervates ____ muscle fibers.

many

39

This is an enzyme that cleaves ACh, producing acetate and choline.

AChE

40

What does GABA do?

it increases chloride permeability in the postsynaptic membrane

41

Name 3 mechanisms for clearing NTs from the synaptic cleft.

  1. diffusion
  2. recycling (pumped out)
  3. destruction

42

When does depolarization at the NMJ begin?

when ACh-gated channels are activated

43

What is AChE?

acetylecholine esterase; an enzyme that cleaves ACh, producing acetate and choline

44

The ACh receptor is a _____ channel.

ligand-gated ion

45

What happens if the safety factor of the synaptic transmission is reduced?

neuromuscular transmission can fail during repetitive activity--> muscle weakness

46

Where is the trigger zone? What does it do?

btw the cell body and the axon; it's where APs arise

47

What is the effect of the CNS synapse?

excitatory OR inhibitory

48

An AP in the inhibitory terminal releases ____, which opens Cl- channels in its target presynaptic terminal.

GABA

49

Where do APs always arise from?

the trigger zone

50

Name 2 receptors that ACh acts upon in the CNS.

  • nicotinic
  • muscarinic

51

A skeletal muscle receives synaptic input from ____ motor neuron.

one

52

What is the transmitter termination for the NMJ?

  • diffusion
  • degradation by esterase

53

The major inhibitory NT in the CNS is _____.

GABA

54

What are dendritic spines?

small protuberances from dendrites that make synaptic contact with incoming axon terminals

55

What is the speed of the CNS synapse?

fast OR slow

56

This is when residual Ca++ builds up inside the nerve terminal from previous APs to allow increased strength of new APs.

facilitation

57

Post-exocytic vesicles are retrieved by the formation of ______.

clathrin coated pits

58

This is the end of the motor axon where it loses its myelin sheath and splays onto the muscle fiber.

the motor end plate

59

What is the difference btw Myasthenia gravis and myasthenic syndrome?

  • Myasthenia gravis = post-synaptic block
  • myasthenic syndrome = pre-synaptic block

60

Why do APs arise at the trigger zone?

the threshold is lower here bc of the high density of voltage-gated Na+ channels

61

An AP in the inhibitory terminal releases GABA, which ______ in its target presynaptic terminal.

opens Cl- channels

62

What happens to ACh?

  • it diffuses out it's destroyed by ACh0
  • it is re-taken up

63

Why is the ACh-gated ion channel called a Non-Selective Cation (NSC) channel?

it is permeable to ALL cations

64

Binding of ACh (the ligand) opens the gate and Na+ ions flow into the muscle fiber to _____ it.

depolarize

65

CNS neurons receive synaptic input from _____ neurons.

many

66

What is the strength of the CNS synapse?

weak

67

In skeletal muscle only, the postsynaptic membrane is _____ to increase surface area.

folded

68

Dx?

  • an autoimmune disease
  • Abs to ACh receptors
  • results in profound weakness upon exertion

Myasthenia gravis

69

How does the AP propogate all the way to the tendon?

voltage-gated Na+ channels open in both directions away from each other

70

The binding of Ca++ triggers the fusion of ____ of the vesicle and surface membranes, opening a _____.

lipids; fusion pore

71

A single AP in the motor axon causes every muscle fiber to twitch ____.

once

72

This is the depletion of releasable synaptic vesicles, reducing the strength of new APs.

synaptic depression

73

What is the transmitter termination for the CNS?

  • reuptake
  • diffusion

74

What is an EPSP?

an excitatory post-synaptic potential; product of the stimulation of the excitatory input that causes depolarization

75

A postsynaptic response can be either ____ or ____.

excitatory; inhibitory

76

Binding of ACh (the ligand) opens the gate and ____ ions flow into the muscle fiber to depolarize it.

Na+

77

During repetitive nerve stimulation, what 2 important and opposing changes occur in the presynaptic terminal?

  • the Ca++ ion concentration builds up
  • the pool of releasable vesicles is depleted