Molecular cell biology Flashcards

1
Q

What are ionotropic receptors?

A

Ligand-gated ion channel

Ion channel opens in response to binding of specific ligands to extracellular sites

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2
Q

The main excitatory neurotransmitter in the CNS?

A

Glutamate

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3
Q

The main inhibitory neurotransmitter in the CNS?

A

GABA

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4
Q

What are the two main types of Ach receptors?

Their features?

A

Nicotinic receptors

  • G protein coupled
  • Slow metabolic response

Muscarinic receptors

  • Ligand-gated ion channels
  • Fast synaptic transmission
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5
Q

How are Nicotinic Ach receptors arranged? (molecular make-up)

A

5 subunits arranged around a central channel

Have 2 or more alpha subunits

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6
Q

What are the two main types of nicotinic receptor sub-units?

A

Heteromeric (different subunits - at least to alpha)

Homomeric (one subuit - has to be one type of alpha)

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7
Q

How do non-depolaraising muscle relaxants work?

A

Block neuromuscular transmission by binding competitively at the agonist site on the muscular nAChR.

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8
Q

Two main types of ionotropic glutamate receptors?

A

NMDA receptor

AMPA receptor

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9
Q

What drug specifically binds to NMDA receptors?

A

Ketamine

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10
Q

Main effects of GABA on the brain, specifically in the amygdala?

A

Calming effects (amygdala commonly associated with emotion)

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11
Q

Two types of GABA receptors?

A

GABAa - ionotropic

GABAb - metabotropic (G-protein coupled)

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12
Q

Results of activation of a GABA receptor?

A

Influx of Cl- thereby inhibiting the neurone

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13
Q

The molecular makeup of a GABA receptor?

A

Heteropentameric (5 different subunits)

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14
Q

Common drugs that act on the GABA receptor?

How do they work?

A

Benzodiazepines, sedatives e.g. phenobarbital, barbituates

They bind on a different subunit to the one that GABA binds on but increase GABA’s action.

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15
Q

How do benzodiazepines increase GABA’s action?

A

They lock the GABA receptor into a position where GABA has a much higher affinity for the GABA receptor.

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16
Q

How do the two glutamate receptors AMPA and NMDA interact?

A

AMPA is activated my small amounts of glutamate release, whereas NMDA is not, it is blocked by a magnesium ion.

AMPA receptors let Na+ into the post-synaptic membrane, depolarising it (as usual)

If there is a large enough glutamate release the NMDA receptor will be activated and the magnesium plug removed

NMDA receptors also let Ca2+ into the post-synaptic membrane, the Ca2+ has a number of secondary effects and increases the post-synaptic membranes ability to be depolarised. It does this through:

  • Increasing the amount of AMPA receptors
  • Phosphorylates AMPA receptors (increases the amount of Na+ that can travel in)

Synapse is said to be enhanced

This contributes to long term potentiation