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Neuroscience > NEUR 0010 - Chapter5 > Flashcards

NEUR 0010 - Chapter5 Flashcards

1
Q

What do electrical synapses do?

A

Allow direct transfer of ionic current from one cell to the next through gap junctions

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2
Q

Where do electrical synapses occur?

A

At gap junctions

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3
Q

What is a gap junction?

A

Six connexins (special proteins) form a connexon, and a connexon from each of two cells combines to form the gap junction

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4
Q

How do electrical synapses differ from most chemical synapses?

A

They’re bidirectional; current can pass just as well either way

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5
Q

What does it mean for two cells to be electrically coupled?

A

That they’re connected by gap junctions through which electrical current can pass

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6
Q

What advantages does electrical coupling offer?

A

Very fast and reliable signal transmission; almost instantaneous

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7
Q

Electrical synapses are very common in which part of the mammalian nervous system?

A

CNS: in almost every part

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8
Q

What happens when an action potential occurs in the presynaptic neuron of an electrically coupled pair?

A

A small amount of ionic current flows across the gap junction channels into the postsynaptic neuron, triggering a small postsynaptic potential

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9
Q

What is a PSP?

A

Postsynaptic potential: induced by the small amount of current that flows from pre to postsynaptic neuron when the presynaptic neuron experiences an action potential

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10
Q

How do PSPs illustrate bidirectionality of electrical synapses?

A

An action potential in Neuron 1 induces a PSP in Neuron 2, but when Neuron 2 undergoes its own action potential, it also induces a PSP in Neuron 1

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11
Q

What is the connection between PSPs induced by presynaptic neurons and action potentials in the postsynaptic neuron?

A

The PSP itself probably isn’t big enough to trigger an action potential in the postsynaptic neuron, but the postsynaptic neuron is often receiving a lot of PSPs from multiple presynaptic neurons, and the cumulative effect can trigger the action potential (synaptic integration)

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12
Q

What function makes gap junctions particularly necessary/prevalent?

A

Needing the neighboring neuron activity to be highly synchronized; very common during early embryonic stages

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13
Q

What is the majority of synaptic transmission in mature human nervous system, electrical or chemical?

A

Chemical

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14
Q

What separates the pre and post synaptic membranes at chemical synapses?

A

Synaptic cleft: filled with matrix of fibrous extracellular protein to bind the two membranes together

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15
Q

What are the two kinds of vesicles usually found in the presynaptic neuron at a chemical synapse?

A

Synaptic vesicles (smaller, carry neurotransmitters) and secretory granules (also called dense-core vesicles; contain soluble protein; appears dark in electron microscope)

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16
Q

What are secretory granules?

A

The larger counterpart to synaptic vesicles: carry soluble protein; also called dense-cored vesicles

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17
Q

What are membrane differentiations?

A

Dense accumulation of protein adjacent to and within pre and postsynaptic membranes of chemical synapses

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18
Q

What are the membrane differentiations on the presynaptic side of a chemical synapse?

A

Active zones: proteins jutting into cytoplasm of terminal, look like pyramids; actual sites of neurotransmitter release

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19
Q

What is the actual site of neurotransmitter release?

A

The active zones: little pyramids of protein along the terminal membrane; the presynaptic membrane differentiation

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20
Q

What is the membrane differentiation on the postsynaptic side of a chemical synapse?

A

Postsynaptic density; contains neurotransmitter receptors (convert intercellular chemical signal to intracellular signal)

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21
Q

What is the postsynaptic density?

A

The membrane differentiation of the postsynaptic membrane; contains neurotransmitter receptors

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22
Q

How does one distinguish the different types of synapse in the CNS?

A

Based on what part of the neuron is postsynaptic to the axon terminal, and based on whether the pre and postsynaptic membrane differentiations are symmetrical or not

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23
Q

What is an axodendritic synapse?

A

When the postsynaptic membrane is on a dendrite

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24
Q

What is an axosomatic synapse?

A

When the postsynaptic membrane is on the cell body

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25
Q

What is an axoaxonic synapse?

A

When the postsynaptic membrane is on the axon of another neuron

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26
Q

Can dendrites ever form synapses with other dendrites?

A

Only in very specialized situations; called dendrodendritic synapses

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27
Q

What is Gray’s type 1 synapse?

A

When the membrane differentiation on the postsynaptic side is thicker than the presynaptic side; postsynaptic density thicker than the active zones; usually excitatory

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28
Q

What is Gray’s type 2 synapse?

A

When the membrane differentiation on the pre and postsynaptic sides are equally thick: postsynaptic density and active zones are symmetrical; usually inhibitory

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29
Q

Which synapse type is usually more excitatory, Gray’s type 1 or type 2? Inhibitory?

A

Gray’s type 1 (asymmetrical) is excitatory; Gray’s type 2 (symmetrical) is inhibitory

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30
Q

What is a neuromuscular junction?

A

When chemical synapses occurs between the axons of motor neurons of the spinal cord, and skeletal muscle; the synaptic junction is outside of the CNS

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31
Q

What is the action potential relationship in neuromuscular junctions?

A

Very fast, and an action potential in the presynaptic motor neuron ALWAYS causes an action potential in the muscle cell it innervates

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32
Q

Why is neuromuscular synaptic transmission so reliable?

A

Large junction: presynaptic terminal contains large number of active zones, and postsynaptic membrane of the muscle (motor end-plate) contains lots of junctional folds that are packed with receptors

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33
Q

What is the motor end-plate?

A

The postsynaptic membrane of a neuromuscular junction on the muscle cell’s membrane; contains many junctional folds that have high neurotransmitter receptor density

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34
Q

What are the three main chemical categories of neurotransmitters?

A

Amino acids, amines, and peptides

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35
Q

What is the difference in storage/secretion of amino acid/amine neurotransmitters vs peptide neurotransmitters?

A

Amino acid/amine are small and are stored in synaptic vesicles; peptide are larger and thus are stored in secretory granules (dense-core vesicles)

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36
Q

What are the three main amino acid neurotransmitters?

A

GABA, glutamate, glycine

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37
Q

What are six main amine neurotransmitters?

A

ACh, Epi, NE, DA, histamine, serotonin

38
Q

What are nine main peptide neurotransmitters?

A

CCK, somatostatin, dynorphin, enkephalins, NAAG, Neuropeptide Y, Substance P, thyrotropin-releasing hormone, VIP

39
Q

What three neurotransmitters mediates fast synaptic transmission in most CNS synapses?

A

GABA, glutamate, and glycine (GABA, Glu, Gly)

40
Q

What neurotransmitter mediates fast synaptic transmission at all neuromuscular junctions?

A

Acetylcholine (ACh)

41
Q

Why are glutamate and glycine abundant in most neurons, whereas GABA and amines are only made in neurons that release them?

A

Because Glu and Gly are protein building block amino acids, so all cells use them anyway

42
Q

How are most AA/A neurotransmitters manufactured?

A

Synthesizing enzymes for amino acid/amine neurotransmitters are transported to axon terminal; transporter proteins then concentrate the manufactured NT into synaptic vesicles

43
Q

How are most peptide NTs manufactured?

A

On ribosomes of RER in the soma: long string of aa’s split in the Golgi, and one of the smaller peptide fragments is the active NT; secretory granules bud off from the Golgi and travel to the axon terminal

44
Q

What triggers NT release?

A

Arrival of an AP in the axon terminal; depolarization causes voltage-gated calcium channels in active zones to open: huge influx of Ca++, which signals release of NT from synaptic vesicles

45
Q

Why is exocytosis of synaptic vesicles so quick after depolarization causes Ca++ voltage-gated channels to open?

A

Because the Ca++ floods in through the active zones, where a whole bunch of synaptic vesicles are already waiting to unleash their neurotransmitter wrath upon the synaptic cleft; some think they’re “docked” at the active zone

46
Q

What is “docking” of synaptic vesicles during chemical synaptic transmission?

A

When the synaptic vesicle’s membrane proteins and the active zone interact; at high Ca++ concentration, the proteins alter conformation to fuse the vesicle membrane and active zone membrane

47
Q

How does release of peptide NT differ from release of AA/A NT?

A

Still occurs by exocytosis with Ca++ changes, BUT doesn’t have to occur at the active zones: happens further away, which is why release of peptide NT requires high-frequency trains of action potentials, so that Ca++ can build up enough to reach it

48
Q

Why is peptide NT release slower than AA/A NT release?

A

Because the secretory granules aren’t docked at the active side; release by exocytosis further away, and require high-frequency action potentials to build up enough Ca++ to reach it

49
Q

What kind of action potentials are required for release of peptide NT?

A

High frequency, so that Ca++ build up can reach the secretory granule docking sites

50
Q

What are the two main types of NT receptors?

A

Transmitter-gated ion channels, and G-protein coupled receptors

51
Q

What are transmitter-gated ion channels?

A

NT receptors: membrane-spanning proteins, four/five subunits to form a pore; binding of an NT causes conformational change to open the pore

52
Q

Which shows more ion selectivity, transmitter-gated ion channels, or voltage-gated ion channels?

A

Voltage-gated; transmitter-gated show less selectivity

53
Q

What does it mean for an NT to be excitatory?

A

It opens channels to allow an influx of Na+, bringing the neuron closer to action potential threshold; depolarization

54
Q

What two ions are ACh-gated channels permeable to?

A

Na+ and K+, they’re not too picky

55
Q

What is an EPSP?

A

Excitatory PSP: transient postsynaptic membrane depolarization caused by the presynaptic release of NT

56
Q

Synaptic activation of what two transmitter-gated channels causes EPSP?

A

ACh and glutamate

57
Q

What does it mean for an NT to be inhibitory?

A

It opens channels to allow an influx of Cl-, bringing the neuron further from action potential threshold; hyperpolarization

58
Q

What is an IPSP?

A

Inhibitory PSP; transient hyperpolarization of the postsynaptic membrane potential caused by presynaptic release of NT

59
Q

Synaptic activation of what two transmitter-gated channels causes IPSP?

A

GABA and glycine

60
Q

Which has faster chemical synaptic transmission, transmitter-gated ion channels or G-protein coupled receptors?

A

Transmitter-gated ion channels, mediated by AA/A NTs

61
Q

What are the characteristics/benefits of G-protein coupled receptors over transmitter-gated ion channels?

A

Slower, and allow for more diverse postsynaptic actions

62
Q

What are the three steps in G-protein coupled receptor action?

A

NT molecules bind to receptor proteins in postsynaptic membrane; receptor proteins activate small G-proteins to move along intracellular fact of postsynaptic membrane; activated G-proteins activate effector proteins

63
Q

What are effector proteins in G-protein coupled receptor transmission?

A

Can be G-protein gated ion channels; can be enzymes that synthesize second messengers, that can trigger additional enzymes and regulate ion channel function and alter cell metabolism and all that jazz

64
Q

Why are G-protein coupled receptors called metabotropic receptors?

A

Because they can activate pathways that trigger widespread metabolic effects

65
Q

How can you explain the inhibitory/excitatory effects of ACh on the heart vs skeletal muscles?

A

ACh acts on G-protein coupled receptors in the heart (slow hyperpolarization by way of K+ channel)), but acts on ACh-gated ion channels in skeletal muscle (rapid depolarization, by way of Na+ channel)

66
Q

What are autoreceptors?

A

Presynaptic receptors that are sensitive to the NT released by the presynaptic terminal; typically G-protein coupled receptors that stimulate second messenger formation

67
Q

What is the common effect of autoreceptors?

A

Inhibition of neurotransmitter release, and potentially neurotransmitter synthesis; allows presynaptic terminal to regulate itself

68
Q

What type of receptor is usually involved in autoreceptors, transmitter-gated ion channels or G-protein coupled receptors?

A

G-protein coupled receptors, usually stimulate second messenger formation

69
Q

What are four ways NT can be cleared from the synaptic cleft?

A

Diffusion away; reuptake by the presynaptic neuron (can be repackaged or dissembled); reuptake by the glia; destroyed in the cleft itself

70
Q

How is ACh removed from the neuromuscular junction?

A

Destruction in the cleft by acetylcholinesterase, released by the muscle cells

71
Q

What happens if ACh isn’t removed from the neuromuscular junction?

A

The transmitter-gated channels close anyway, and persists; desensitization: neuromuscular transmission fails

72
Q

How do receptor antagonists work to inhibit synaptic transmission?

A

Bind to receptors and block the normal action of the transmitter

73
Q

What does curare do the synaptic transmission?

A

Receptor antagonist: blocks the receptors from binding to ACh in skeletal muscle

74
Q

How do receptor agonists work?

A

Instead of inhibiting synaptic transmission, just mimic: bind to and activate receptors

75
Q

What does nicotine do the synaptic transmission?

A

Receptor agonist: mimics ACh in skeletal muscle (specifically, binds to nicotinic ACh receptors)

76
Q

What does it mean that postsynaptic EPSPs at a given synapse are quantized?

A

They’re multiples of the quantum, the number of transmitter molecules in a singly synaptic vesicle and the number of postsynaptic receptors available

77
Q

What is a miniature PSP?

A

The tiny response to spontaneously released NT by exocytosis in the absence of presynaptic stimulation

78
Q

What is quantal analysis, and what is it used for?

A

Method of comparing mini PSP amplitudes to evoked PSPs: determines how many vesicles released NT during synaptic transmission

79
Q

What is the difference in NT release at neuromuscular junctions vs in the CNS?

A

At neuromuscular junction, hundreds of vesicles are released for an EPSP for 40mV or more; in the CNS, maybe only one vesicle will be released, for a much smaller EPSP

80
Q

What are the two types of EPSP summation?

A

Spatial and temporal

81
Q

What is spatial EPSP summation?

A

Adding together EPSPs that are generated simultaneously by many different synapses on a dendrite

82
Q

What is temporal EPSP summation?

A

Adding together EPSPs generated at the same synapse when they occur in rapid succession (kind of snowballing)

83
Q

What determines the effectiveness of an excitatory synapse in triggering an action potential?

A

How far the synapse is from the spike initiation zone, and the properties of the dendritic membrane

84
Q

What is the dendritic length constant?

A

The distance where the depolarization of the dendritic membrane is 47% of that at the origin; based on logarithms; index of how far depolarization can spread down a dendrite or axon

85
Q

What does the dendritic length constant depend on?

A

Internal resistance (resistance to current flowing longitudinally) and membrane resistance (resistance to current flowing across the membrane)

86
Q

How do internal and membrane resistance affect the dendritic length constant?

A

Higher internal resistance decreases the dendritic length constant; higher membrane resistance increases the dendritic length constant (prevents “leaks”)

87
Q

What do internal and membrane resistance depend on?

A

Internal resistance depends on dendrite diameter; membrane resistance depends on the number of ion channels open

88
Q

What does the term “excitable dendrites” mean?

A

That transmission of depolarization down the dendrite to the spike initiation zone doesn’t just depend on internal/membrane resistance; they have voltage-gated ion channels that can amplify small PSPs and “snowball” them towards the spike initiation zone, too

89
Q

What is shunting inhibition?

A

When an inhibitory synapse hyperpolarizes the membrane potential, and represents an influx of negative charge as an efflux of positive charge: shunts the positive current flow (for depolarization) outward across the membrane

90
Q

What is modulation?

A

The type of synaptic transmission that relies on G-protein coupled NT receptors that aren’t directly associated with ion channels; don’t directly evoke EPSP/IPSP, but modify the effectiveness of the EPSPs generated by other synapses with transmitter-gated channels

91
Q

What is an example of modulation using NE in the brain?

A

NE binds to beta receptors: activates G-protein coupled pathway that activates effector protein (adenylyl cyclase) to catalyze AMP into cAMP (second messenger); cAMP stimulates protein kinases to phosphorylate specific sites on cell proteins (in the brain with NE, decreases K+ conductance by closing K+ channels; this increases dendritic membrane resistance and increases length constant)

Neuroscience (19 decks)

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