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ZOOL 342 > Synaptic Transmission 1 > Flashcards

Synaptic Transmission 1 Flashcards

1
Q

difference between electrical synapse and chemical synapse?

A
  • electrical: gap junction connects cells allow current to flow DIRECTLY between cells
  • chemical: no direct connection between cells; transmitters used to communicate between cells
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2
Q

TRUE or FALSE: In an electrical synapse transmission, the distance between pre and post cell membranes is very large

A

FALSE: very small (~3.5 nm)

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3
Q

TRUE or FALSE: In an electrical synapse transmission, there is cytoplasmic continuity between the cells

A

TRUE

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4
Q

What is implied when we say there is cytoplasmic continuity between cells?

A

can inject current in one cell and see depolarization in the next cell

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5
Q

TRUE or FALSE: In an electrical synapse transmission, current flows through gap junction channels.

A

TRUE

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6
Q

TRUE or FALSE: In an electrical synapse transmission, the agent of information transmission is neurotransmitters.

A

FALSE: ionic currents (not NTs)

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7
Q

TRUE or FALSE: In an electrical synapse transmission, there is a slight synaptic delay.

A

FALSE: virtually no synaptic delay

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8
Q

TRUE or FALSE: In an electrical synapse transmission, transmission is usually unidirectional.

A

FALSE: bidirectional

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9
Q

Describe the structure of a gap junction between neurons

A
  • 2 connexons line up to form gap junction, which acts as a pore that allows ions to pass from one cell to another
  • each connexon is composed of 6 connexins
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10
Q

What is implied when we say that electrical synaptic transmission is bidirectional?

A

current injection into either cell A or B results in depolarization in both cells (i.e. cells are electrically coupled)

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11
Q

TRUE or FALSE: In chemical synaptic transmission, the distance between pre and post cell membranes is large.

A

TRUE: 20-40 nm

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12
Q

TRUE or FALSE: In chemical synaptic transmission, there is cytoplasmic continuity between the cells.

A

FALSE: no cytoplasmic continuity

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13
Q

TRUE or FALSE: In chemical synaptic transmission, the agent of information transmission is ionic currents

A

FALSE: chemical transmitters

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14
Q

TRUE or FALSE: In chemical synaptic transmission, there is virtually no synaptic delay

A

FALSE: significant synaptic delay of ~1.5 ms

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15
Q

What causes the synaptic delay in a chemical synaptic transmission?

A

activity of pre-synaptic Ca2+ channels slowly opening

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16
Q

TRUE or FALSE: In chemical synaptic transmission, transmission is unidirectional

A

TRUE

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17
Q

In terms of where synapses occur, what is the difference between excitatory and inhibitory synapses?

A
  • excitatory synapses occur on dendrites and dendritic spines
  • inhibitory synapses occur on dendrites CLOSE TO THE CELL BODY or on the cell body itself
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18
Q

What is the function of dendritic spines?

A
  • offer greater surface area for synapses
  • compartmentalize information if necessary
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19
Q

Where are postsynaptic densities (PSD) most often found?

A

excitatory synapses

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20
Q

TRUE or FALSE: PSD is found at both excitatory and inhibitory synapses.

A

TRUE

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21
Q

What is the function of the PSD?

A
  • provide structural matrix which clusters ion channels, and anchors signaling molecules such as kinases and phosphatases
  • general organizer of the postsynaptic signal transduction machinery
  • links regulatory molecules to their targets
  • coordinates developmental and activity-dependent changes in postsynaptic structures
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22
Q

Where do synapses occur in the PNS?

A

neuromuscular junction (NMJ)

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23
Q

What is special about the NMJ that is different for synapses in the CNS?

A

NMJ has a high safety factor

i.e. ratio of pre:post-synaptic AP = 1:1 in NMJ (PNS)

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24
Q

What is curare? Which receptor does it bind to? How does it affect this receptor? What is its function? Where does it act?

A
  • plant alkyloid
  • block nAChRs
  • prevents nerve transmission at the NMJ (i.e. reduce AP in muscles)
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25
Q

How does a postsynaptic potential travel along a muscle fiber?

A

passive membrane properties

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26
Q

TRUE or FALSE: As the electrode is moved further from the endplate, the PSP gets larger and larger, as it approaches the Nav-gated channels.

A

FALSE: smaller and smaller until it reaches the Nav-gated channels, where threshold is reached and a full AP is generated

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27
Q

TRUE or FALSE: ACh receptors are located very close to/directly at the NMJ

A

TRUE

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28
Q

TRUE or FALSE: nAChRs are always post-synaptic membrane

A

TRUE

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29
Q

Which other drug is similar to curare, in the sense that it blocks nAChR?

A

alpha-bungarotoxin

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30
Q

What is the main difference between curare and alpha-bungarotoxin?

A
  • curare: can be easily removed (competitive antagonist)
  • alpha-bungarotoxin: cannot be removed
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31
Q

Where are ACh receptors found in the synaptic cleft? V-gated Na+ channels?

A
  • ACh receptors: at the folds of the cleft
  • V-gated Na+ channels: at the base of the folds
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32
Q

Which ions flow (and in which direction) after ACh binds to nAChR?

A
  • Na+ flows in
  • K+ flows out

(cause depolarization)

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33
Q

What should we look at on a graph to determine which ion is flowing?

A

reversal potential

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34
Q

What is the reversal potential of the synaptic current at the NMJ? Explain.

A
  • reversal potential of ~0 mV
  • because nAChR allows both Na+ and K+ to flow (multiple ions flowing at once)
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35
Q

What kind of current occurs at positive vs negative voltages in synaptic event at the NMJ?

A
  • positive voltage = outward current
  • negative voltage = inward current
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36
Q

What is another name for the current at the NMJ?

A

endplate current

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37
Q

Describe the shape of the endplate current. Draw it. Explain it.

A
  • sharp onset followed by exponential decay to baseline (slide 20)
  • sharp onset occurs because all the channels are activated/open simultaneously
  • exponential decay occurs because the channels close at different times
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38
Q

What is meant when we say the current at the NJMJ is probablistic?

A

nAChRs open at the same time, but close at different times

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39
Q

What are the main excitatory ionotropic receptors? Which NT binds to them?

A

NMDARs and AMPARs; glutamate

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40
Q

Which ionotropic receptor is kainate similar to?

A

AMPAR

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41
Q

What are the main differences between AMPA and NMDA?

A
  • Ca2+ clows through NMDA
  • Mg2+ block in NMDA
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42
Q

how does NMDA get unblocked?

A

once both ampa and nmda bound, AMPA opens faster, causing depolarization –> this depolatization unblocks Mg2+ in NMDA

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43
Q

How many transmembrane helices make up one subunit of the nACh, Gly, GABA, and 5-HT receptors? How many subunits are needed to form a receptor?

A

4 transmembrane helices pre subunit; 5 subunits per receptor

44
Q

How many transmembrane helices make up one subunit of the Glu receptors? How many subunits are needed to form a receptor?

A

3 transmembrane helices plus pore loop; 4 subunits per receptor

45
Q

What is different about the amino and carboxy terminus in nACh, Gly, GABA, 5-HT, and Glu receptors?

A
  • nACh, Gly, GABA, 5-HT have an external amino AND carboxy terminus
  • Glu has an external amino terminus and INTERNAL carboxy terminus
46
Q

How many glutamate molecules can AMPA bind? How many are needed for activation?

A
  • can bind 4
  • only need 2 for activation
47
Q

Which AMPAR subunit confers Ca2+ impermeability? which site specifically? why does this site cause Ca2+ impermeabitlity?

A

GluR2; Q/R site; arginine (R) in GluR2 (i.e. large positive side chain)

(whereas GluR1,3,4 have glutamine (Q))

48
Q

Why are most AMPARs impermeable to Ca2+?

A

GluR2 subunit confers Ca2+ impermeability

49
Q

Which type of receptor is involved in epilepsy, ALS, pain, and addiction?

A

Ca2+ PERMEABLE AMPARs

50
Q

What kind of subunits make up NMDARs? How many of each subunit? Which transmitters bind to which subunit?

A
  • 2 NR1; glycine
  • 2 NR2; glutamate
    (note: 4 subunits total)
51
Q

Which transmitters and how many are required for activation of NMDARs?

A

2 glycine and 2 glutamate

52
Q

NMDARs act as “coincidence detectors”. What does this mean?

A

they require both NTs and depolarization to be activated

53
Q

TRUE or FALSE: AMPARs are coincidence detectors

A

FALSE: NMDARs

54
Q

What are the main differences in properties conferred by different subunits of the NMDAR?

A
  • length of time channels remain open
  • conductance
55
Q

Which subunit causes the NMDAR to open for longer, causing a larger current?

56
Q

TRUE or FALSE: receptors are linked with other proteins that keep them functioning properly

57
Q

What are the main inhibitory receptors? Which ions flow across the membrane when these receptors are activated?

A

glycine and GABA receptors; Cl-

58
Q

How do the Glycine and GABA receptors cause direct inhibitory transmission?

A
  • activation of these receptors causes opening of Cl- channels
  • keep cell at Cl- equilibrium potential –> causes hyperpolarization which prevents depolarization
59
Q

TRUE or FALSE: all glycine receptors are metabotropic

A

FALSE: ionotropic

60
Q

In general, describe the structure of a GlyR.

A
  • combination of alpha and beta subunits
  • scaffolding protein known as gephyrin
61
Q

Where does gephyrin bind?

A

associates with beta subunit of a GlyR

62
Q

How many and which subunits compose a homomeric GlyR?

A

5 alpha subunits

63
Q

How many and which subunits compose a heteromeric GlyR?

A

2 alpha subunits + 3 beta subunits

64
Q

How many types of GlyR alpha subunits are there? beta subunits?

A
  • 4 types of alpha (a1, a2, a3, a4)
  • 1 type of beta
65
Q

TRUE or FALSE: neonatal animals express the alpha1 subunit, but this changes throughout development such that older animals express the alpha2 subunit

A

FALSE: first express alpha2, then express alpha1

66
Q

Where does glycine bind of the GlyR, in terms of subunits?

A

interface between the alpha and beta subunits

67
Q

How many molecules of glycine are required to activate GlyR? How many can bind in total?

A
  • 2 required
  • if homomeric, can bind 5 (bc 5a subunits)
  • if heteromeric, can bind 4-?
68
Q

What is a potent antagonist of GlyRs?

A

strychnine

69
Q

Why do neontae have alpha2 subunits in GlyR, whereas adults have alpha1?

A
  • alpha2 causes a longer “open time”
  • as development proceeds, the time open gets shorter –> ALLOWS BETTER CONTROL OF THE SYSTEM
70
Q

What are the 2 major kinds of GABA receptors? Which GABARs correspond to these types?

A
  • ionotropic = GABAa, GABAc
  • metabotropic = GABAb
71
Q

Which 2 substances inhibit GABARs? (antagonists)

A

picrotoxin and bicucilline

72
Q

TRUE or FALSE: all GABARs are ionotropic

A

FALSE: some ionotropic and some metabotropic

73
Q

make a summary chart of all the receptors, their types, which ions, which NTs, etc.

A

make the chart

74
Q

What are 4 types of drugs that affect GABAa receptors?

A
  1. GABAa antagonists (picrotoxin and bicuculline)
  2. barbiturate (pentobarbital)
  3. benzodiazepines
  4. alcohol
75
Q

What is the effect of picrotoxin on GABAa receptors?

A

pore blocker; bind and reduce GABAa ipsps

76
Q

What is the effect of bicuculline on GABAa receptors?

A

competitive antagonist; bind and reduce GABAa ipsps

77
Q

What side effects do GABAa antagonists cause?

A

convulsions

78
Q

What is the effect of barbiturates on GABAa receptors?

A

addictive; lengthen the OPEN TIME of receptor channels

79
Q

What is the effect of benzodiazepines on GABAa receptors? Is it less or more addictive than barbiturates?

A
  • less addictive
  • increase the NUMBER of channels opening (and how often they open)
80
Q

What is the effect of alcohol on GABAa receptors?

A

potentiates ipsps –> calming and sedation

81
Q

Which drugs reduce GABAa ipsps? enhance?

A
  • reduce: picrotoxin, bicuculline
  • enhance: barbiturates, benzodiazepines, alcohol
82
Q

TRUE or FALSE: activation of neonatal GABA receptors hyperpolarize the cell membrane

A

FALSE: depolarize

83
Q

How does activation of neonatal GABARs affect NMDA receptors? Describe the 3 steps.

A
  • depolarize
  • unblock NMDA receptors
  1. Cl- leaves the cells via GABAa receptors
  2. depolarization
  3. unblock NMDAR
84
Q

TRUE or FALSE: The equilibrium potential for Na+ changes during development

A

FALSE: Cl-

85
Q

How does the equilibrium potential for Cl- change during development?

A

gets more negative

86
Q

TRUE or FALSE: GABA is excitatory in neonates and inhibitory in adults

87
Q

Why does the equilibrium potential for Cl- get more negative throughout development? What is the approxiamte Ecl in nenonates and humans?

A
  • in neonates, high lecels of NKCC1, high Cl- inside the cell –> ~-40 mV
  • in adults, low levels of NKCC1, high levels of KCC2, low Cl- inside the cell –> ~-75 mV
88
Q

What is the theory that explains why we need a greater expression of NKCC1 in neonates?

A

Ca2+ is necessary for developmental processes in neonates

89
Q

Draw excitatory activation, direct inhibition, and shunting inhibition.

A

slides 43-45

90
Q

What is shunting inhibition?

A

reduce amplitude of EPSP –> EPSP not large enough to depol to threshold and CANNOT CAUSE AP

91
Q

What are 2 mechanisms of inhibition?

A
  1. direct: maintain membrane potential away from threshold via increasing Cl- or K+ conductance
  2. shunting: EPSP is ‘reduced’ and is not strong enough to depolarize the cell to threshold
92
Q

What is the relationship between the membrane potential of the presynaptic cell and the amount of transmitter release? Consider the membrane potential.

A

presynaptic cell has to be depolarized to ~50 mV or greater to cause Ca2+ channels to open –> NT release

93
Q

TRUE or FALSE: there is no delay between the presynaptic AP and the PSP

A

FALSE: there is a delay

94
Q

What is the only requirement for transmitter release?

A

an increase in intracellular Ca2+ (and a presynaptic depolarization to open the Ca2+ channels)

95
Q

What is the minimum amount of transmitter that can be released?

A

a quanta; thousands of transmitter molecules

96
Q

What is another name for the contents in one vesicle

97
Q

What is spontaneous release? How does this happen? What does it lead to?

A
  • release of transmitter into the synaptic cleft in the absence of a presynaptic AP
  • b/c sometimes, there is enough unbound Ca2+ in the presynaptic cell
  • leads to miniature postsynaptic potentials at the NMJ called MINIATURE ENDPLATE POTENTIALS (MEPPS)
98
Q

How does vesicle recycling occur?

A
  1. clathrin-coated pits are present near the active zone
  2. they bind to the surface of vesicles
  3. they pull the vesicles back into the cell
99
Q

What does SNARE stand for?

A

snap receptors

100
Q

What does the SNARE complex do?

A

help vesicles fuse with membrane during transmitter release

101
Q

What are the major SNARE proteins invovled in vesicle fusion? Be specific.

A
  • vesicle proteins (v-SNAREs): synaptobrevin
  • membrane proteins (t-SNAREs): syntaxin, SNAP-25
102
Q

What does the t in t-SNAREs stand for?

A

TERMINAL synaptic membrane

103
Q

How does the SNARE complex facilitate vesicle docking, fusion, and release of transmitter?

A
  • Ca2+ binds to synaptotagmin and triggers membrane fusion
  • COMPLEXIN helps to keep formation in place
  • COMPLEXIN IS LOST, SNARE proteins interact and bring vesicles and presynaptic membrane closer together
104
Q

tetanus vs botulinum:
- produced by which bacteria?
- mechanism? which specific proteins?
- effects?

A

TETANUS:
- Clostridium tetani
- cleaves SNAREs (synaptobrevin) in inhibitory INs that synaps onto motor neurons (disinhibition)
- strong complete contraction of mm

BOTULINUM:
- Clostridium botulinum
- cleaves SNAREs (synaptobrevin, SNAP-25, syntaxin) in various neurons including motor neurons
- relaxation of mm

105
Q

List the sequence of events involved in transmission

A
  1. transmitter is synthesized and then stored in vesicles
  2. an AP invades the presynaptic terminal
  3. depolarization of presynaptic terminal causes opening of V-gated Ca2+ channels
  4. influx of Ca2+
  5. Ca2+ causes vesicles to fuse with presynaptic membrane (via binding to synaptotagmin)
  6. NT released into synaptic cleft via exocytosis
  7. transmitter binds to receptor molecules in postsynaptic membrane
  8. opening or closing of postsynaptic channels (close if NT unbinds)
  9. postsynaptic current causes +/- PSP that changes excitability of postsynaptic cell (passive spreading)
  10. retrieval of vesicular membrane from plasma membrane

ZOOL 342 (21 decks)

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