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neuroscience and mental health LCRS > lecture 6: neurotransmitters > Flashcards

lecture 6: neurotransmitters Flashcards

1
Q

what are the essential components before a neurotransmitter is released?

A
  1. the dendrites detect the input
  2. the information propagates down the dendrite and is integrated in the soma
  3. the action potential is generated in the axon hillock
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2
Q

how big is the synaptic cleft?

A

the synaptic cleft is 20 -100 nm wide

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3
Q

how long down it take for one action potential to get from one cell to the next?

A
  • it takes 2 milliseconds
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4
Q
  • what is the overall mechanism of a neurotransmitter
A
  1. the action potential propagates along the membrane
  2. the voltage gated calcium channels open
  3. the Ca2+ enters the nerve terminal and the exocytosis of the NT starts
  4. the neurotransmitter diffuses across the gap and interacts with the receptors
  5. the transmitter is removed by being broken down by enzymes at the post synaptic synapse

the sodium potassium pump restores the membrane potential

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5
Q

what are the three classes of neurotransmitter?

A
  • amino acids
  • amines
  • neuropeptides
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6
Q

when does integration happen and what does it do?

A

integration is when the neurone receives multiple transmitter influences which are integrated to produce diverse functional responses

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7
Q

what is essential for the release of neurotransmitters?

A

calcium is vital

the increase in Ca2+ is needed

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8
Q

how does rapid release neurotransmitter occur?

A
  • the NT are either diced at the synapse or they are floating in the terminal region
  • interaction between presynaptic membrane and vesicle proteins allowing the vesicle to be docked stably
  • there are alpha helical structures which interact together to form a super helix
  • this has made a stable complex of the vesicle at the synapse which is full of neurotransmitter
  • the vesicle then awaits Ca2+ signal
  • when it comes the complex undergoes a conformational change which drives the release of the transmitter into the synaptic cleft
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9
Q

what naturally occurring toxins have an effect on the synaptic vesicle proteins?

A
  • Tetanus - inhibits transmitter release
  • Botulinum - flaccid paralysis
  • Alpha Latrotoxin -depletes NT
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10
Q

what are the three main steps of transmitter release?

A
  • docking (vesicles on pre synaptic membrane)
  • protein complex formation (between vesicle membrane and cytoplasmic protein)
  • ATP and vesicle recycling
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11
Q

what is the nature of ion channel receptors?

A
  • the response is fast
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12
Q

what are neurotransmitters at ion channel receptors at the CNS?

A
  • glutamate

- GABA

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13
Q

what are neurotransmitters at ion channel receptors at the neuromuscular junction?

A
  • acetylcholine
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14
Q

what is the nature of G protein coupled receptors?

A
  • slow
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15
Q

what are neurotransmitters at G protein coupled receptors at the CNA and PNS?

A
  • acetylchpline
  • dopamine
  • noradrenaline
  • 5 - hydroxytryptamine
  • neuropeptides
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16
Q

what is glutamate for?

A
  • excitatory

- needed for the influx of Cl-

17
Q

what are the two types of glutamate receptor?

A
  • AMPA receptor

- NMDA receptor

18
Q

what is the AMPA receptor needed for?

A
  • responsible for the majority of FAST excitatory synapses
19
Q

what is the NMDA receptor for ?

A
  • this is the slow component
  • it needs two inputs for the receptor to become activated
  • the membrane needs to be depolarised
  • the glutamate needs to bind
  • the NMDA activation is dependent on the depolarisation of the cell
  • this also lets in the calcium
20
Q

what is the GABA for ?

A

GABA is inhibitory and it allows the influx of the Cl-

21
Q

what is the overall glutamate excitatory synapse mechanism?

A
  • glutamate interacts with receptors and causes the entry of Na and Ca through the NDMA receptor

– transporters on the pre synaptic membrane and on the GLIAL cells cause the uptake of glutamate

  • once in the glial cells or the neurones the glutamate is inactivated by glutamine synthesise to make glutamine
22
Q

what is the main transporter that uptakes glutamate?

A

EAAT2

23
Q

what his epilepsy caused by?

A
  • this is causes by the abnormal release of glutamate leading to the hyper excitability of the cells
24
Q

whats the overall GABA inhibitory synapse mechanism?

A
  • GABA is the main inhibitory NT
  • GABA binds to the receptor and allows the entry Cl- which hyper polarises the cell
  • there are transporters on the glial cells and pre synaptic neurone which take up the GABA
  • once the GAba has been taken up it is inactivated by the GABA transaminase which makes succinate semialdehyde which feeds into the TCA cycle
25
Q

what is the transporter which takes up the GABA?

A

GAT

gaba transporters

26
Q

compare the structures of GABA and glutamate?

A

they have very similar structures

- the removal of the carboxyl group in the glutamate makes GABA

27
Q

how can we make anti epilepsy medication?

A
  • by exploiting the GABA receptor we can make anti epileptics, sedatives and muscle relaxants
  • there is a receptor for Benzodiazepines (anxiety and insomnia)

and
- there is a receptor for Barbiturates

anti epilepsy drugs are trying to combat excess glutamate therefore makes more GABA by converting more glutamate into GABA by decarboxylating it

so we can use glutamic acid decarboxylase

neuroscience and mental health LCRS (13 decks)

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