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NEUR231 Neurobiology > Synaptic Transmission > Flashcards

Synaptic Transmission Flashcards

1
Q

What neurotransmitter is released at all post-ganglionic parasympathetic neurons?

A

ACh

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2
Q

What is another name for an electrical synapse?

A

Gap junction

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3
Q

What are 2 examples of electrical synapses in vertebrates?

A

-Cerebral cortex inhibitory neurons (often dendrodendritic)

-hippocampus (linking into other networks with electrical synapses)

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4
Q

Describe the structure of a gap junction

A

Comprised of 2 adjacent connexons (1 transmembrane in each cell membrane).
Connexon is comprised of 6 connexin subunits

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5
Q

What is an advantage of electrical synapses compared to chemical synapses?

A

Due to being electrically coupled, the time delay between depolarisation of adjacent cells is negligible, allowed neurons to synchronize activity

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6
Q

Describe the intracellular environment of a presynaptic terminal

A

-Lots of mitochondria
-secretory granules (having been transported soma along microtubules)
-Synaptic vesicles (full of NT)

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7
Q

How large is a chemical synapse?

A

The gap is ~5nm

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8
Q

What is notable about the post-synaptic membrane?

A

post-synaptic density - this is where all the receptors are localised

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9
Q

What are the “Classic” neurotransmitter types?

A

Amino acid or amine NTs

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10
Q

Where are classic neurotransmitters synthesised

A

All synthesis in the axon terminal

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11
Q

Describe the process of chemical synaptic signaling

A
  1. NT synthesised & stored in vesicles
  2. AP generated in presynaptic neuron, travelling to terminal
  3. Opening of voltage-gated Ca++ channels, influx of Ca++
  4. Ca++ causes exocytosis of vesicles
  5. NT released & diffuses across the synaptic cleft
  6. NT binds to receptors on the post-synaptic membrane
  7. Shutdown of transmission [ie enzymatic activity in synaptic cleft, or active transport into presynaptic terminal etc]
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12
Q

How much NT is contained per vesicle?

A

roughly ~200 molecules of NT HOWEVER this can be pharmacologically influenced

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13
Q

how many receptors can a single type of NT bind to?

A

A single type of NT can bind to many different types of receptors

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14
Q

What are 5 different CNS synapse morphologies and where you might find these?

A

Axodendritic [classic]
Axosomatic [many via gPCRs]
Axoaxonic [inhibitory NT system]
Axospinous [dynamic plasticity, learning & memory]
Dendrodendritic [many electrical synapses]

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15
Q

What type of synapse is this?

A

Axodendritic chemical synapse

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16
Q

What type of synapse is this?

A

Axosomatic chemical synapse

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17
Q

What type of synapse is this?

A

Axoaxonic chemical synapse

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18
Q

Give a common scenario with this synapse type and the role of each neuron

A
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19
Q

What is axon branching and an example of where this can be found?

A

When an axon splits to multiple terminals (to the same or different postsynaptic cell). Classical example is neuromuscular junction.

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20
Q

What ae the 2 types of synapses when categorised by membrane differentiation?

A

Gray’s type I: asymmetrical (large postsynaptic density), usually excitatory

Gray’s type II: symmetrical (pre & post synaptic densities equal), usually inhibitory

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21
Q

What are the 3 categories of neurotransmitter?

A

Amino Acid, Amines and Peptides

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22
Q

How many classic NTs are there?

A

9

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23
Q

What are the 3 Amino Acid type neurotransmitters?

A

GABA, Glutamate (Glu) and Glycine (Gly)

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24
Q

What is GABA?

A

Gamma-aminobutyric acid, major inhibitory NT in the brain

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25
Q

What is the role of Glutamate?

A

Major excitatory NT

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26
Q

What is the role of glycine?

A

inhibitory NT in the brainstem/spinal cord

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27
Q

What are the 6 Amine type NTs?

A

Acetylcholine (ACh)
Dopamine (DA)
Epinephrine
Histamine
Norepinephrine
Serotonin (5-HT)

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28
Q

How many NT types can a single neuron synthesise?

A

a single neuron will only synthesise a SINGLE classic NT (ie glutamergic will only ever be glutamergic) BUT many neuropeptides can be co-released

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29
Q

What NTs can cause rapid changes in the post-synaptic membrane potential and how?

A

-Amino Acid NTs (by opening ion channels)
-ACh (via nicotinic receptors)
-Serotonin (via ionotropic receptors)
[all other amine types only act through gPCRs]

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30
Q

What receptor types can bind with ALL classic NTs?

A

gPCRS (metabotropic receptors)

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31
Q

Describe the action of neuropeptides

A
  • They are signaling molecules
    -they all act at gPCRs
    -all neuromodulators
    -co-released with a “classic” NT
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32
Q

Where are neuropeptides synthesised and why?

A

At the Soma because it leverages the cellular machinery for peptide creation.

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33
Q

How do neuropeptides get to the terminal?

A

Once synthesised, gets packaged into secretory granules and actively transported to the terminal along microtubules

34
Q

What is required for Classic NT synthesis?

A

Precursor molecule + synthesizing enzyme

35
Q

Generally describe the process of NT release by exocytosis

A
  • vesicle is docked & ready at the membrane
    -AP arrives at the terminal
    -VGCCs open
    -influx of Ca++
    -binds with docking protein & causes conformational change
    -vesicle “dragged” to the membrane & binds
    -NTs released into the cleft
36
Q

What is the key mechanism of NT release?

A

Exocytosis is stimulated by intracellular [Ca++].

(There are many ways to increase [Ca++], not just VGCCs.

The [Ca++] is the key.

37
Q

How many proteins are involved in synaptic vesicle release and recycling?

A

more than 30

38
Q

Name the key proteins circled here

A
39
Q

What is the function of clathrin?

A

protein in presynaptic terminal, coats the “used” vesicle

40
Q

What is the function of dynamin?

A

protein in presynaptic terminal, “pinches” off the vesicle from the membrane (so it can be filled with NT)

41
Q

What is the function of synapsin?

A

protein in presynaptic terminal, keeps filled vesicles together

42
Q

What is the function of NSF & SNAPs?

A

proteins in presynaptic terminal responsible for priming of docked vesicles

43
Q

what is the function of SNAREs?

A

Proteins in the presynaptic terminal, formed when a vesicle is primed & thought to be involved in fusion of vesicle to membrane

44
Q

What is the function of synaptotagmin?

A

Senses Ca++ and pulled the vesicle into the membrane. It is the Ca++ sensor for exocytosis.

45
Q

What processes in the presynaptic terminal are Ca++ dependent?

A

-Exocytosis of vesicles
-priming of vesicles

46
Q

What are SNARE proteins comprised of?

A

-Synaptobrevin (on the vesicle membrane)

-syntaxin
-SNAP 25 (both on the pre-synaptic membrane)

47
Q

Describe what happens to SNARE proteins with Ca++ influx

A

Ca++ influx causes synaptobrevin/syntaxin/SNAP-25 to form SNARE complex & vesicle is then primed & docked at the membrane

At the next Ca++ influx, synaptotagmin binds Ca++ & conformational change pulls the vesicle into the membrane

48
Q

What is the result of synaptotagmin gene deletion?

A

Lethal mutation

49
Q

Name each component in this diagram and the process being shown

A
50
Q

What is the mechanism of botox & tetanus toxins?

A

They interfere with formation of SNARE complex and prevent release of NT

51
Q

What is the structure of transmitter-gated ion channels?

A

5 transmembrane domains

52
Q

What is a reversal potential?

A

The membrane potential where ionic current can reverse (ie go the opposite direction). This applies to generic channels ie ionotropic channels

53
Q

What is the reversal potential?

A

For a single ion channel, Vr = equilibrium potential for that ion

If 2-ion channel, Vr = somewhere between the equilibrium potentials of the 2

54
Q

What is EPSP

A

Excitatory post-synaptic potential - transient post-synaptic membrane depolarisation

55
Q

What is IPSP

A

inhibitory post-synaptic potential - transient post-synaptic membrane hyperpolarisation

56
Q

Describe the general steps of EPSP generation

A

-AP down the presynaptic neuron
-release of NT
-NT binds to post-synaptic neuron
-causes influx of Na+ in post-synaptic cell
-causes depolarising change in post-synaptic membrane potential (potentially moving closer to threshold for AP)

57
Q

Describe the general steps of IPSP generation

A

-AP down pre-synaptic neuron
-release of NT
-NT binds to post-synaptic receptor
-causes Cl- influx in post-synaptic cell
-causes hyperpolarising change in post-synaptic membrane potential

**Note that we are NOT getting a Cl- flow at resting Vm, this would be in a cell that has already been depolarised - only then can we get IPSP using Cl- channel

58
Q

What are the 2 types of post-synaptic receptors

A

ionotropic
metabotropic

59
Q

Describe how gPCRs are neuromodulators

A

Because they will NEVER depolarise a membrane to threshold. They just make it easier or harder by moving Vm closer/further away from threshold.

60
Q

What is the resulting action of gPCRs?

A

Activation of enzyme & second messenger systems, or G protein gated ion channels (indirectly open ion channel)

61
Q

Describe autoreceptors and their function

A
  • receptors on pre-synaptic axon terminal membrane (sometimes found on presynaptic cell dendrites)
    -bind to the same NT that the neuron releases
    -often inhibit further NT release (negative feedback loop)
    -seem like a safety valve
62
Q

What are 4 different ways to limit NT signalling & an example of each?

A

-Diffusion away from synapse [example - astrocytes uptake glutamate]

-Reuptake via active transport [SSRIs work by decreasing reuptake]

-Enzymatic breakdown in synaptic cleft [MAO inhibitors work by decreasing degradation in terminal]

-Desensitization to deactivate the NT [AChE cleaves ACh in cleft to render it inactive]

63
Q

What is synaptic integration?

A

the process by which multiple synaptic potentials combine within one postsynaptic neuron

64
Q

what is neural computation?

A

The processing of thousands of neural inputs

65
Q

What is quantal theory?

A

how much NT has to be released to causes EPSP

66
Q

What is quantal analysis?

A

The process of determining the number of vesicles that release during neurotransmission

67
Q

What is the elementary unit of synaptic transmission?

A

synaptic vesicle

68
Q

What is MEPP and what is the significance of it’s discovery?

A

Mini End Plate Potential - significance is that is suggests spontaneous release of NT vesicles that are NOT associated with depolarisation of pre-synaptic membrane - NOT due to calcium influx. This suggests they are “accidents” where vesicles randomly bumped into the membrane & released.

69
Q

What is EPSP summation?

A

integration/adding together many EPSP to produce significant post-synaptic depolarisation

70
Q

What are 2 ways of integrating EPSPs?

A

Spatial: multiple EPSP at SAME TIME but DIFFERENT locations

Temporal: Multiple EPSP in RAPID SUCCESSION at the SAME LOCATION

71
Q

What is the active role of dendrites?

A

They actively shunt a potential towards the trigger zone using voltage gated channels

72
Q

What are 2 examples of ways an IPSP can move Vm away from theshold?

A

-can bring in Cl-
-can take out K+

73
Q

What is the result of pharmacological agents that block parasympathetic activity?

A

Blocking parasympathetic activity mimics sympathetic activity

74
Q

What determines the effect of a released NT?

A

The receptor it binds to - receptor subtypes can cause different effects when binding to the same NT

75
Q

What receptor subtypes does ACh bind to?

A

-nicotinic receptor
-muscarinic receptor

76
Q

What receptor subtypes does norepinephrine bind to?

A

α receptor
β receptor

77
Q

What receptor subtypes does Glutamate bind to?

A

AMPA
NMDA
Kainate

78
Q

What receptor subtypes does GABA bind to?

A

GABA_A
GABA_B

79
Q

Why is the active properties of dendrites important?

A

Because of signal decay in the cable model, spread of synaptic potential to the soma would be affected

80
Q

How do inhibitory synapses shunt the synaptic current?

A

As an AP flows along a dendrite/axon, the inhibitory synapse can be generating an IPSP that prevents the AP flowing to the soma/axon hillock

NEUR231 Neurobiology (11 decks)

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