Synaptic Transmission Flashcards

1
Q

What is a neuromuscular junction?

A

The connection point of a motor neurons axon onto the muscle fibre

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2
Q

What is the vesicle structure inside the synapse? What is its function?

A

A ball like structure which is where the neurotransmitter is stored before release

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3
Q

Where is the synapse located?

A

At the end of an axon

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4
Q

What does the action potential do to the vesicle structure inside the synapse?

A

It causes it to release its neurotransmitters stored inside the vesicle

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5
Q

Where do the neurotransmitters stored in the vesicles get released to?

A

To the synaptic cleft

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6
Q

What is the synaptic cleft?

A

space between the pre and post synaptic membranes

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7
Q

What about the action potential in the synaptic vesicle causes the neurotransmitter to be released?

A

It opens up Ca2+ voltage gated ion channels

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8
Q

What does the Ca2+ do to assist in neurotransmitter release? Where does the Ca2+ go?

A

Causes the vesicle membranes to merge with the pre-synaptic membrane which leads to exocytosis of the neurotransmitter <> Goes into the synapse

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9
Q

What does the neurotransmitters do once in the synaptic cleft?

A

Interacts with the post-synaptic membrane activating ligand gated receptor channel complexes on their surface

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10
Q

What does the ligand gated receptor channel complex open up when activated? What flows through it?

A

Opens non-selective cationic channels <> All cations (e.g. Na+, K+, Ca2+)

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11
Q

What happens to the post-synaptic membrane when the neurotransmitter activates the ligated gated receptor channel complex on it? What movement of particles causes the membrane to depolarise?

A

It causes the post-synaptic membrane to depolarise <> Na+ goes in, K+ goes out

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12
Q

What is the depolarisation of the post-synaptic membrane called?

A

End plate potential (EPP)

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13
Q

What can the end plate potential then do on the muscle tissue?

A

If it reaches the threshold potential then it will activate Na+ gated ion channels resulting in an action potential being generated that propagates away (in both directions) from the synapse

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14
Q

What can the end plate potential then do on the muscle tissue?

A

If it reaches the threshold potential then it will activate Na+ gated ion channels resulting in an action potential being generated that propagates away (in both directions) from the synapse

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15
Q

What is the time delay from an action potential arriving at the synapse to the generation of an action potential in the muscle tissue?

A

0.5ms

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16
Q

What is the neurotransmitter inside the vesicles of the synapse?

A

Acetylcholine (ACh)

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17
Q

Under what circumstances would an action potential in the synapse cause a supra-threshold potential in the post-synaptic membrane?

A

It will always generate a supra-threshold potential resulting in an action potential

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18
Q

What happens after an action potential is generated by the post-synaptic membrane?

A

It propagates through the muscle tissue

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19
Q

What are the two types of chemical synapses isn’t eh CNS?

A

Excitatory synapse and inhibitory synapses

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20
Q

What does depolarisation of the excitatory synapse cause?

A

Depolarisation of the post synaptic membrane result in the Excitatory postsynaptic potential (EPSP)

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21
Q

What does depolarisation of the inhibitory synapse cause?

A

Hyper-polarisation of the postsynaptic membrane called the inhibitory postsynaptic potential (IPSP)

22
Q

Label the diagram of the process of synaptic activation

23
Q

What are the neurotransmitters that mediate excitatory synapses?

A

Mainly glutamic acid/glutamate or ACh

24
Q

What is glutamate?

A

An amino acid

25
What is the ionic mechanic of excitatory postsynaptic potentials (EPSPs)?
Transient opening of ligand gated Na+, K+ and sometimes Ca2+ channels
26
What are the neurotransmitters that mediate inhibitory synapses?
Mainly GABA (gamma-aminobutyric acid) or glycine
27
What is the ionic mechanic of inhibitory postsynaptic potentials (EPSPs)?
Usually transient opening of ligand gated K+ channels
28
What are the classification of neurotransmitters?
Small molecule neurotransmitters and Neuropeptides
29
What are the characteristics of small molecule neurotransmitters?
Small molecules that usually fast action and direct on the post synaptic receptors
30
What are some examples of small molecule neurotransmitters?
Amino acids (i.e. glutamate, GABA, glycine etc.), Acetylcholine (ACh) and Amines (serotonin etc.)
31
What are the characteristics of neuropeptides?
Large molecules that have an indirect (i.e. metabotropic) action on postsynaptic receptor or regulatory (i.e. modulatory) action and are slow to react: second to minutes
32
What are some examples of neuropeptides?
Neuropeptide Y, Substance P, Kisspeptin, Enkephaln (remember 2)
33
What are the factors determining synaptic actions?
Type of neurotransmitter/modulator \<\> The type of neurotransmitter receptor in the postsynaptic membrane \<\> The amount of neurotransmitter receptor expressed in the postsynaptic membrane (synaptic plasticity)
34
How can the type of receptor affect the function of the neurotransmitter? Give an example with glutamate
Different types of receptors process the neurotransmitter differently \<\> i.e. Glutamate has four different types of receptors: Kainate, NMDA, AMPA and Metabotropic glutamate receptor (it is indirectly activated by a messenger molecule) \<\> Kainate, AMPA and NMDA are all cationic non-selective ion channel but Kainate and AMPA are permeable to K+ and Na+ only while kainite is also permeable for Ca2+
35
What is calcium important for?
The release of neurotransmitter in the synapse \<\> Contraction of muscles
36
What are the levels of calcium in the brain measured in?
Low µmolL-1
37
What happens if too much glutamate is released?
Causes too much Ca to go through NMDA receptor causing excessive depolarisation and over activation of neurons
38
What happens when there is long-term opening of NDMA receptors?
Causes excessive Ca2+ entry into neurons which damages them by excitotoxicity
39
What are some diseases caused by excitotoxicity?
Parkinsons, alzheimers
40
How is the neurotransmitter inactivated?
It diffuses away form the synapse \<\> Enzymatic degradation \<\> Re-uptake and recycling
41
What enzyme can degrade ACh? Where does this degradation occur?
Acetylcholine esterase in the synaptic cleft
42
What is the re-uptake of neurotransmitters more common for?
Amino acids and amines
43
How are neurotransmitters re-absorbed? What is this called?
Neurotransmitter transports int eh pre-synaptic membrane or the adjacent glia cells \<\> Glutamate transporter
44
What kind of CNS component is particular important in re-uptaking glutamate into the synapse?
Astrocytes
45
What are axon initial segments covered in lots of?
Na+ voltage gated channels
46
What is the function of dendrites?
To increase the surface area of synaptic contacts
47
Up to how many synaptic contacts might there be on a nerve cell?
Tens of thousands
48
How does a nerve cell integrate thousands of synaptic contacts into a signal?
Due to the temporal and spatial summation of postsynaptic potentials at axon initial segment
49
How do the individual synapses contribute to the activation of an action potential?
Some synapses are excitatory and some inhibitory \<\> The excitatory synapses potential produces only a very small potential (0.1mV) and is a passive current so it degrades as it moves through the dendrites to the cell body \<\> The inhibitory synapses produce an opposite charge reducing the effect of EPSPs
50
How can synapses produce an action potential?
Either by producing a series of rapid frequency EPSPs (TEMPORAL) which accumulate and reach supra-threshold potential OR multiple synapses producing an EPSP (SPATIAL) at the same time again accumulating to reach supra-threshold potential