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Brain and Behaviour Year 2 > CAL 1 > Flashcards

CAL 1 Flashcards

1
Q

What does a cell body of a neurone consist of

A

perikaryon and a nucleus.

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2
Q

where in the neurone is the site of protein synthesis

A

the cell body

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3
Q

What does the cell body of the pre-synaptic neurone give rise to

A

the cell body of the pre-synaptic neurone gives rise to dendrites (apical and basal) and an axon

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4
Q

where does the axon arise from

A

the axon hilliock

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5
Q

what is an IPSP

A

this is an inhibitory post synaptic potential

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6
Q

where do inhibitory inputs synapse onto

A

inhibitory inputs commonly synapse onto the cell body (axosomatic synapses) or the axon (axoaxonic synapses).

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7
Q

what does an IPSP do that inhibits the action potential

A

Activation of an inhibitory input generates a graded hyperpolarization this means that the neurone cannot depolarise to reach the threshold point in order to generate an action potential

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8
Q

What is the major role of the apical dendrites

A

receive excitatory input from other nerve cells

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9
Q

what does an EPSP do

A

this is an excitatory post synaptic potential

- it causes depolarisation and generates an excitatory input

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10
Q

what happens at the axon hilliock in order to generate an action potential

A
  • in order to generate an action potential there is summation at the axon hillock which eventually leads to the threshold point being reached
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11
Q

what concentrations of ions are high intracellular then extracullularly

A

intracellularly - potassium, protein negatively charged (anions) are higher

extracellularly - sodium and chloride are higher

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12
Q

The resting nerve cell membrane has a high relative permeability to

A

potassium

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13
Q

what is the typical resting potential

A

-65mv, this approximates to the potassium equilibrium potential

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14
Q

what is the resting potential of a neurone due to

A

potassium leaking out of the non gated potassium channels

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15
Q

what is the equilibirum potential for sodium

A

this is the membrane potential at which there is no net flux of sodium across the membrane
+58mv

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16
Q

what are the two groups that central nervous system neurotransmitters are classified as

A
  • peptide

- non peptide

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17
Q

name some peptide neurotransmitters

A
  • somatostatin
  • substance P
  • Cholecytokinin
  • enkephalins
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18
Q

name some non peptide neurotransmitters

A
  • dopamine
  • glutamate
  • acetylcholine
  • GABA
  • noradrenaline
  • 5-HT
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19
Q

what are the types of non peptide neurotransmitters

A
  • Monoamine
  • amino acid
  • choline esters
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20
Q

name some examples of non peptide neurotransmitters

A
  • Monoamine - dopamine, 5HT, noradrenaline
  • amino acid- glutamate, GABA
  • choline esters - acetylcholine
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21
Q

describe how peptide neurotransmitters are synthesised

A
  • starts with synthesis of peptide neurotransmitters
  • this happens via transcription of the genes in the cell body nucleus, then translation in the cytoplasm
  • this forms the large precursor molecule
  • the precursor molecule undergoes translational maturation and cleavage
  • then transported to the pre-synaptic terminal via fast axonal transport
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22
Q

describe how non peptide neurotransmitters are synthesised

A
  • these are synthesised in the presynaptic terminal from precursor molecules
  • the precursor molecules are taken up by active transport process into the terminal
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23
Q

are there more peptide or non peptide molecule

A

non peptide - these are gene products so are more susceptible to evolutionary change

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24
Q

where are both peptide and non peptide molecules stored

A

they are both stored in vesicles following entry by active transport processes

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25
Q

describe what happens at the presynaptic terminal causing it to release neurotransmitters

A
  • action potential causes the membrane to depolarise
  • this depolarisation opens calcium channels
  • this causes calcium ions to diffuse down there concentration gradient
  • the increase in intracellular calcium ions causes vesicles to fuse with the membrane and release neurotransmitters
  • the neurotransmitters are released
  • they diffuse across the synapse and have an effect on the post synaptic cells
26
Q

what is co-transmission

A

this is when both non-peptide and peptide are released at the same time

27
Q

what is an autoreceptor

A
  • this is a receptor on the pre-synaptic membrane that is the same shape as the neurotransmitter and can either increase or decrease release of the neurotransmitter
28
Q

how is non peptide neurotransmitter terminated

A
  • by active reuptake into the pre-synaptic terminal
29
Q

how are the ways that neurotransmitters can be stopped

A
  • either by reuptake into the pre synaptic terminal

- or degradation by enzymes in the synapse

30
Q

what happens to neurotransmitters that have been reuptaken into the presynaptic terminal

A
  • either degraded or taken back up for storage in the vesicles
31
Q

what are retrograde transmitters

A

these are lipophillic molecules such as nitric oxide that use an uncovenentianal mechanism of transport

  • they are not stored in vesicles but they are syntehsised on demand
  • act as retrograde messengers - released from postsynaptic terminals and act on presynaptic terminals
32
Q

What is the typical synaptic delay (i.e. time between depolarization of the pre-synaptic terminal and the onset of the post-synaptic respons

A

0.5ms

33
Q

What effect will a decrease in extracellular [Ca⁺⁺] have on synaptic transmission?

A

inhibit

34
Q

Approximately how many vesicles are there in each terminal?

A

10,000

35
Q

How rapidly are peptide transmitters transported from the nucleus to the nerve terminal?

A

400mm/day

36
Q

What effect will blockade of the pre-synaptic autoreceptors have on synaptic transmission?

A

unpredictable effect

- depends on the type of neurotransmitter

37
Q

Approximately how many molecules of transmitter are stored in each vesicle?

A

300

38
Q

What effect will an inhibitor of transmitter inactivation have on synaptic transmission?

A

potentiate (increase)

39
Q

In the central nervous system, approximately how many vesicles fuse with the pre-synaptic nerve terminal in response to the influx of Ca⁺⁺ associated with each action potential?

A

between 1-10

40
Q

What effect will blockade of the post-synaptic receptors have on the excitability of the post-synaptic neurone?

A

unpredictable

41
Q

what are the two receptors that neurotransmitters bind to

A
  • ligand gated receptor ion channel

- G protein ion channels

42
Q

what are ligand gated ion channels

A

1) Ligand gated ion channels are heterooligomeric proteins traversing the membrane,

43
Q

How many subunits do ligand gated ion channels consist of

A

often consisting of four or five subunits.

44
Q

how short is the time taken for the neurotransmitter to bind to the ligand gated ion channel and for it to open

A

e time taken for the transmitter molecules to bind and the ion channel to open is short («0.1 msec).

45
Q

what does the duration of channel opening in the ligand gated ion channels depend on

A

The duration of channel opening depends, in part, on the rate of dissociation of the transmitter molecules and the kinetics of channel gating.
- Amino acids induce fast neurotransmitter action in the CNS, but most monoamine and peptide neurotransmitters do not activate ligand-gated ion channels, and thus act more slowly, as neuromodulators.

46
Q

what does a G protein channel consist o f

A

The receptor consists of a single polypeptide chain that traverses the membrane 7 times.

47
Q

describe how a G protein channel works

A
  • single transmitter molecule binds to the G protein and it becomes activated by the displacement of GDP by GTP
  • this causes the dissociation of alpha GTP, beta and gamma subunits
  • Usually α GTP, but often β and gamma as well, stimulates the effector to bring about the response,
  • Return of the G protein to its resting state occurs by α GTP hydrolysing its bound GTP to GDP, with subsequent reassociation with the β and gamma complex
48
Q

The Duration of effects is in msecs applies to…

A

ligand gated ion channels

49
Q

Single polypeptide chain is the typical structure of a:

A

G protein coupled receptor

50
Q

Heterooligomeric protein is the typical structure of

A

ligand gated ion channel

51
Q

This receptor type requires 2 molecules of transmitter for activation

A

ligand gated ion channel

52
Q

2nd messengers can mediate the effects of

A

G protein coupled receptor

53
Q

This type of receptor consists of a peptide chain that traverses the membrane 7 times

A

G protein coupled receptor

54
Q

what does the amplitude of the EPSP depend on

A

the amplitude of the EPSP depends on the amount of transmitter released, which depends on the number or pre-synaptic fibres activated which, in turn, will depend on the intensity of the stimulus.

55
Q

what happens if the amplitude of the EPSP reaches the threshold

A
  • an action potential will be generated
56
Q

what can membrane depolarisations also result from

A

I) Influx of Ca⁺⁺
II) Closing of K⁺ channels
III) Efflux of Cl⁻

57
Q

What does the action potential result from

A

(i) an unequal distribution of ions across the membrane due to the activity of the Na⁺/K⁺ pump and
(ii) the presence of a population of non gated K⁺ channels which allows K⁺ to leave the cell down its electrochemical gradient (outward K⁺ current).

.

58
Q

describe the characterstics of EPSPs

A
  • localised
  • non propagated potentials result from the transmitter released from the afferent fibres activating a population of ligand gated ion channels
59
Q

what voltage is the depolarisation sufficient enough to open voltage gated sodium channels and trigger an action potential

A

At about -55mV (threshold), the depolarization is sufficient to open voltage gated Na⁺ channel, hence triggering an action potential.

60
Q

what usually causes inhibition of an action potential

A

Inhibitory transmitters usually combine with post-synaptic receptors to open channels permeable to Cl⁻ causing a hyperpolarization (Inhibitory Post-synaptic Potential, IPSP).

The opening of channels permeable to Cl⁻ and K⁺ usually mediates synaptic inhibition.

61
Q

what does the amplitude of the IPSP depend on

A

the amplitude of the IPSP depends on the amount of transmitter released which depends on the number of pre-synaptic fibres activated which, in turn, will depend on the intensity of the stimulus.

62
Q

what happens if you have excitation and inhibitory inputs

A

have an EPSP of reduced potential

Brain and Behaviour Year 2 (36 decks)

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