Neurotransmission 1 - Kenyon Flashcards

1
Q

What allows ions to move between cells to create electrical transmission?

A

gap junctions

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2
Q

Cells connected by gap junctions are (blank) coupled

A

electricaly

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3
Q

Do electrically coupled cells have the same membrane potential?

A

Yes

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4
Q

Can action potentials travel in both directions across a synapse?

A

Yes!

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5
Q

Can subthreshold activity be conducted bidirectionally?

A

Yes!

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6
Q

In what tissues is electrical coupling of significant importance?

A
  1. CNS neurons
  2. Cardiac muscle
  3. smooth muscle
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7
Q

Can a synaptic vesicle contain more than one type of neurotransmitter?

A

yes!

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8
Q

When an action potential is fired presynaptically, what are the three possible changes to the postsynaptic membrane potential?

A
  1. Hyperpolarization
  2. Depolarization
  3. No change
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9
Q

Depolarization of presynaptic terminals causes opening of voltage gated (blank) ion channels

A

Ca

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10
Q

Does calcium flow in or out after activation of voltage gated channels?

A

IN

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11
Q

what does Ca do to the presynaptic terminal?

A

it causes vesicle fusion with the membrane

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12
Q

By what process are neurotransmitters released from membrane fused vesicles?

A

Exocytosis

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13
Q

What are the two general processes of removal of neurotransmitter from the cleft?

A

Glial uptake or enzymatic degradation

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14
Q

Postsynaptic current causes (blank) or (blank) postsynaptic potential that changes the excitability of the postsynaptic cell

A

excitatory or inhibitory

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15
Q

Is calcium necessary AND sufficient to cause neurotransmission?

A

YES

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16
Q

Na channel inhibitors block what step in neurotransmission? (lidocaine)

A

action potential

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17
Q

Lambert-Eaton and conotoxin block the influx of what ion?

A

Ca

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18
Q

botulinum and tetanus block what step of neurotransmission?

A

Vesicle release

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19
Q

Curare, benzo’s, and myasthenia gravis do what to receptors?

A

Activate OR inactivate them

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20
Q

What two drugs block the inactivation or uptake of neurotransmitters?

A

Prozac and physotigmine

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21
Q

Name the five general groups of small neurotransmitters

A
  1. ACh
  2. Glutamate
  3. GABA and glycine
  4. Biogenic amines (Nepi, ,Epi, dopamine, serotonin, histamine)
  5. ATP, ADP, AMP, adenosine
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22
Q

What are the three unconventional neurotransmitters?

A
  1. Nitric oxide
  2. Carbon monoxide
  3. Endocannabinoids
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23
Q

during, synthesis of small molecule neurotransmitters, where are enzymes synthesized in the neuron?

A

Cell body

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24
Q

Where are small molecule neurotransmitters synthesized and packaged in the neuron?

A

terminal

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25
Q

Transport of enzymes and NEUROPEPTIDES from the cell body to the terminal are moved down (blank) tracks

A

microtubule

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26
Q

Where are neuropeptide precursors modified to produce active neuropeptides?

A

Terminal

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27
Q

Are small molecules or neuropeptides transported “slowly” down the axon?

A

small molecule

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28
Q

Once small molecules are broken down in the cleft, what happens with their components?

A

They are reabsorbed by the presynaptic neuron and recycled

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29
Q

What happens to the neuropeptides in the cleft after they do their job?

A

They diffuse out of the cleft or are degraded by proteolytic enzymes

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30
Q

What unconventional neurotransmitter has a Ca dependent enzyme in its synth?

A

Nitric oxide

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31
Q

What enzyme is Ca dependent for nitric oxide?

A

NO synthase

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32
Q

NO acts on what membrane bound effector protein?

A

guanylyl cyclase

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33
Q

Are unconventional neurotransmitters highly permeable?

A

yes!

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34
Q

What is the precursor to NO?

A

ARRRRRRginine

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35
Q

What is the “old school” criteria to define a neurotransmitter? (3)

A
  1. substance must be present presynaptically in vesicles
  2. Substance release must be triggered by increase in presynpatic Ca concentration
  3. Specific receptors for the substance must be present postsynaptically
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36
Q

What is the “new school” criteria to define a neurotransmitter?

A
  1. The substance can be synthesized “on demand” (unconventional neurotransmitters).
  2. The substance can be synthesized “on demand” by Ca2+-activated enzymes and diffuse out of the presynaptic cell
  3. Specific receptors for the substance can be present in the cytoplasm of the postsynaptic cell
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37
Q

Is ALL nuerotransmitter release Ca dependent?

A

YES YES YES

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38
Q

Vesicle membranes recycling is mediated by what type of endocytosis?

A

Clathrin-mediated endocytosis?

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39
Q

What are the three proteins needed in vesicle recycling?

A
  1. Synaptotagmin
  2. SNAREs
  3. Ca channel
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40
Q

Explain “kiss and run” vesicle fusion

A

Only a small pore opens up between the membrane and vesicle, instead of the whole vesicle fusing, allowing for rapid vesicle recyling

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41
Q

What is quantal release of a neurotransmitter?

A

Vesicle fuses and dumps all its contents into the cleft

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42
Q

What effect will removal of extracellular Ca or blockage or lowering Ca entry presynaptically have on neurotransmitter release?

A

it will be reduced

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43
Q

Is the role of Ca in skeletal muscle the same as it is in cardiac or smooth muscle?

A

NO

44
Q

Agatoxin and conotoxin act on Ca channels in what cells?

A

Nerve terminals and dendrites and neuroendocrine cells

45
Q

What is the idea of co-transmission?

A

One neuron can release more than one type of neurotransmitter

46
Q

What are the two factors necessary to release a neuropeptide instead of a small molecule?

A
  1. Higher frequency of presynaptic APs

2. Higher elevation of intracellular Ca

47
Q

Will the release of neuropeptides also stimulate the release of small molecules simultaneously?

A

Yes!

48
Q

Where are small molecules ejected?

A

Into the synaptic cleft

49
Q

Where are neuropeptides ejected?

A

They’re squirted out all over the damn place

50
Q

Ca binds at what protein during vesicle fusion?

A

Synaptotagmin

51
Q

What SNARE is found on the vesicle?

A

synaptobrevin

52
Q

What SNARE is found in the plasma membrane?

A

syntaxin

53
Q

Is synaptotagmin on the vesicle or the plasma membrane?

A

Vesicle, strangely enough

54
Q

does postsynaptic membrane PERMEABILITY change DURING synaptic transmission?

A

yes

55
Q

In the Nernst equation ion concentration gradient is essentially equal to (blank)

A

voltage

56
Q

the (blank) of a cell membrane to a given ion determines the contribution of that ion to the membrane potential

A

permeability

57
Q

If Pk (permeability to K) is large, Em (membrane conductance) is close to (blank)

A

Ek (conductance of K)

58
Q

if PNa (permeability to Na) is large, Em (membrane conductance) is close to (blank)

A

ENa (conductance of Na)

59
Q

does the Nernst equation work with divalent ions?

A

NOOOOOPE, just monovalent (K, Na, Cl, NOT CALCIUM)

60
Q

What physical change in the plasma membrane sets permeability to an ion?

A

Opening or closing of ion channels

61
Q

Is there such a thing as gradual opening of ion channels?

A

No, they are either fully open or fully closed

62
Q

Describe the steps in ion passage through an ionotropic receptor?

A
  1. Neurotransmitter binds TO THE CHANNEL
  2. Channel opesn
  3. Ions flow into cell
63
Q

Describe the steps in ion passage through a metabotropic receptor?

A
  1. Neurotransmitter binds to a G PROTEIN
  2. G protein is activated
  3. G protein subunits move to an effector protein
  4. Intracellular messengers from effector proteins activate the ion channel
  5. Ions flow into the cell
64
Q

If channels highly selective for Na open, what happens to PNa?

A

it increases!

65
Q

Does PNa move to EQUAL ENa?

A

NO, it just moves TOWARD ENa

66
Q

The larger the increase in PNa, the (blank) it becomes to ENa

A

closer

67
Q

Nonselective channels move membrane potential to what value?

A

0 mM!!!

68
Q

What potential is halfway between ENa and Ek?

A

0!!

69
Q

the reversal potential is the (blank) potential associated with opening a particular channel

A

target

70
Q

For a highly selective channel Erev is the (blank) potential of the chosen ion.

A

Nernst equilibrium

71
Q

For a poorly or non-selective channel Erev will be (greater than, less, than, betwen) the Nernst equilibrium potentials of the ions that pass through the channel.

A

between

72
Q

Opening a channel will shift the membrane potential towards the (blank) potential.

A

reversal

73
Q

The more channels you open the closer the membrane potential will move to (blank)

A

Erev

74
Q

What happens to the membrane potential of -65mV when you open nonselective channels?

A

It becomes less negative

75
Q

What happens to the membrane potential of +65mV when you open nonselective channels?

A

It becomes more negative

76
Q

If the membrane potential is already 0mV, what happens if you open a nonselective channel?

A

it stays the same!!

77
Q

The action of a neurotransmitter drives the postsynaptic potential towad (blank) for the particular ion channels being activated

A

Erev (target potential)

78
Q

The value of (blank) is determined by the relative permeability of the channels to Na+, K+, Ca2+, Cl-,

A

Erev

79
Q

The main channels activated by neurotransmitters to generate receptor potentials are (blank) for monovalent cations, or (blank) for divalent ions

A

nonselective, selective

80
Q

If the target potential is positive, the action potential is a (blank)

A

EPSP

81
Q

If the target potential is negative, the action potential is a (blank)

A

IPSP

82
Q

An EPSP makes the postsynaptic neuron (more/less) likely to fire an AP

A

more

83
Q

What neurotransmitter is used for EPSPs?

A

glutamate! Think MSG and chinese restaurant syndrome and getting super wired!

84
Q

What neurotransmitter is used for IPSPs?

A

GABA. That’s why its in OTC sleep meds!

85
Q

An IPSP makes the postsynaptic neuron (more/less) likely to fire an AP

A

less

86
Q

Can an IPSP still cause a depolarization of membrane potential?

A

Yes, as long as the Erev remains below the threshold.

87
Q

Ion channels nonselective for cations or selective for Ca ions mediate (blank)

A

EPSPs

88
Q

Ion channels selective for K mediate (blank)

A

IPSPs

89
Q

Ion channels selective for Cl mediate (blank) if Ecl is negative to threshold or (blank) if ECl is positive to threshold

A
  1. IPSPs

2. EPSPs

90
Q

Erev>threshold= (blank)

A

excitatory

91
Q

Erev<threshold= (blank)

A

inhibitory

92
Q

Can a neuron sum input from thousands of inputs?

A

YES

93
Q

Will one AP at one synapse cause an EPSP to reach threshold

A

Hellllll no!

94
Q

Will one AP at one synapse cause an end plate potential at a nueromuscular junction to reach threshold?

A

Good god yes!

95
Q

It takes (multiple/single) APs at (multiple/single) synapses for an EPSP to reach threshold

A

multiple, multiple

96
Q

Can APs arrive at different times and still be summed to generate an EPSP?

A

NO, they have to arrive at nearly the same time

97
Q

What is the effect of the summation of suprathreshold EPSPs and an IPSP?

A

the IPSP will drag the summed EPSPs down towards the target potential of the inhibitory signal

98
Q

Is the summation of EPSPs and IPSPs linear?

A

NO

99
Q

Can postsynaptic neurons signal back to the presynaptic neuron?

A

YES

100
Q

What are the retrograde transmitters? (4)

A
  1. Nitric Oxide
  2. Carbon monoxide
  3. Endocannabinoids
  4. Prostaglandins
101
Q

In retrograde signaling, glutamate causes an increase in (blank) influx leading to a retrograde signal

A

postsynaptic calcium

102
Q

Can a neurotransmitter inhibit its own release?

A

YES

103
Q

Where are the receptors located for neurotransmitter self-regulation?

A

on the presynaptic terminal

104
Q

Are glia important in neurotransmission?

A

Yes, they are involved in clearing the synaptic cleft

105
Q

What current type are the calcium channels used for neurotransmitter release?

A

PQ or N

106
Q

What inhibits PQ calcium channels?

A

agotaxon

107
Q

What inhibits N calcium channels?

A

conotoxin