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z:2017 - Biosci 107 2/2 > Synaptic Transmission > Flashcards

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

A
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
Q

What is the ionic mechanic of excitatory postsynaptic potentials (EPSPs)?

A

Transient opening of ligand gated Na+, K+ and sometimes Ca2+ channels

26
Q

What are the neurotransmitters that mediate inhibitory synapses?

A

Mainly GABA (gamma-aminobutyric acid) or glycine

27
Q

What is the ionic mechanic of inhibitory postsynaptic potentials (EPSPs)?

A

Usually transient opening of ligand gated K+ channels

28
Q

What are the classification of neurotransmitters?

A

Small molecule neurotransmitters and Neuropeptides

29
Q

What are the characteristics of small molecule neurotransmitters?

A

Small molecules that usually fast action and direct on the post synaptic receptors

30
Q

What are some examples of small molecule neurotransmitters?

A

Amino acids (i.e. glutamate, GABA, glycine etc.), Acetylcholine (ACh) and Amines (serotonin etc.)

31
Q

What are the characteristics of neuropeptides?

A

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
Q

What are some examples of neuropeptides?

A

Neuropeptide Y, Substance P, Kisspeptin, Enkephaln (remember 2)

33
Q

What are the factors determining synaptic actions?

A

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
Q

How can the type of receptor affect the function of the neurotransmitter? Give an example with glutamate

A

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
Q

What is calcium important for?

A

The release of neurotransmitter in the synapse <> Contraction of muscles

36
Q

What are the levels of calcium in the brain measured in?

A

Low µmolL-1

37
Q

What happens if too much glutamate is released?

A

Causes too much Ca to go through NMDA receptor causing excessive depolarisation and over activation of neurons

38
Q

What happens when there is long-term opening of NDMA receptors?

A

Causes excessive Ca2+ entry into neurons which damages them by excitotoxicity

39
Q

What are some diseases caused by excitotoxicity?

A

Parkinsons, alzheimers

40
Q

How is the neurotransmitter inactivated?

A

It diffuses away form the synapse <> Enzymatic degradation <> Re-uptake and recycling

41
Q

What enzyme can degrade ACh? Where does this degradation occur?

A

Acetylcholine esterase in the synaptic cleft

42
Q

What is the re-uptake of neurotransmitters more common for?

A

Amino acids and amines

43
Q

How are neurotransmitters re-absorbed? What is this called?

A

Neurotransmitter transports int eh pre-synaptic membrane or the adjacent glia cells <> Glutamate transporter

44
Q

What kind of CNS component is particular important in re-uptaking glutamate into the synapse?

A

Astrocytes

45
Q

What are axon initial segments covered in lots of?

A

Na+ voltage gated channels

46
Q

What is the function of dendrites?

A

To increase the surface area of synaptic contacts

47
Q

Up to how many synaptic contacts might there be on a nerve cell?

A

Tens of thousands

48
Q

How does a nerve cell integrate thousands of synaptic contacts into a signal?

A

Due to the temporal and spatial summation of postsynaptic potentials at axon initial segment

49
Q

How do the individual synapses contribute to the activation of an action potential?

A

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
Q

How can synapses produce an action potential?

A

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

z:2017 - Biosci 107 2/2 (16 decks)

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