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Neuro > GABA and glycine > Flashcards

GABA and glycine Flashcards

1
Q

explain the 2 main methods with which inhibitory mechanisms work

A

with ligand-binding receptors, 2 things can happen once the ion channels open

  1. influx of negatively charged ions
  2. open potassium channels, potassium efflux
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2
Q

name 2 inhibitory neurotransmitters

A

GABA and glycine

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3
Q

inhibitory neurotransmitters eg. GABA cause what?

A

neuronal membrane hyperpolarisation

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4
Q

what do hyper polarisations result in?

A

an influx of negative charge or an efflux of positive charge

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5
Q

GABA is the major…..

A

…..inhibitory neurotransmitter in the central nervous system

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6
Q

GABA synthesis

A

synthesised in nerve terminals from glutamate

  • glutamate decarboxylase converts glutamate to GABA, vitamin B6 acts as a cofactor
  • lose a carboxylic acid when going from glutamate to GABA
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7
Q

why is it clever that GABA is synthesised from glutamate?

A

means that if a cell can make the excitatory neurotransmitter, it will also always be able to make the inhibitory neurotransmitter, ensuring the organism can perform both excitatory and inhibitory effects.

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8
Q

GABA storage

A

transported into vesicles by VIAAT (VGLUT is glutamate equivalent)

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9
Q

shape of GABA vesicles

A

oval

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10
Q

shape of glutamate vesicles

A

round

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11
Q

how does GABA mediate its response?

A

via GABAa and GABAb receptors

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12
Q

GABAa receptor structure and GABA binding

A
  • ligand gated chloride channel
  • pentameric structure (key difference to the glutamatergic ones, which were all tetramers)
  • variety of subunits (6 alpha, 3 beta, 3 gamma, also pi, delta, epsilon)
  • most common configuration is 2 alpha, 2 beta and 1 gamma
  • GABA binds extracellularly at the interface between the alpha and beta receptors (2 interfaces)
  • need 2 molecules of GABA binding to the alpha beta interface in order for channels to open
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13
Q

where are GABAa receptors found?

A

-majority of GABAa receptors are found post-synaptically, but they can be found pre-synaptically and also on various glial subtypes

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14
Q

why is the GABAa receptor the target of many different types of drugs?

A

because it has multiple binding sites

-eg. Benzodiazepine binding sites, alpha gamma interface

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15
Q

GABAb receptor structure

A
  • GPCR
  • extracellular N-terminal “venus flytrap” domain
  • 7 TM region made of alpha helices
  • internal c-terminal domain that interacts with the g-proteins
  • GABA receptor forms dimers, can be heteromers of 2 different subtypes of GABAb
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16
Q

what happens when there is GABAb receptor binding

A

g-protein activation - Gi/o protein cascade
-causes hyper polarisation through 2 effects

  1. opens potassium channels – efflux of positive charge, makes the inside of the cell more negative, hyperpolarisation
  2. blocks VGCC’s, preventing calcium from entering the cell.
17
Q

GABA re-uptake and degradation

A

3 main mechanisms

  1. reuptake of GABA from the synaptic cleft back into the pre-synaptic terminal by high-affinity Na+ dependent GABA re-uptake transporters (GATs), where it can be packaged back up into vesicles by the vesicular inhibitory amino acid transporter (VIAAT)
    - Neurons = GAT-1
    - Glial cells = GAT-3
  2. metabolism of GABA to Succinic acid in the synapse by GABA transaminase
  3. diffuse away from the synapse (can’t exert any actions because no receptor it could act at away from the synapse)
18
Q

what is epilepsy?

A

-unpredictable seizures, a lot of excitation in the brain

19
Q

how is epilepsy treated?

A

-treat it by increasing inhibition
1. GABAa receptor
enhancers
-increasing amount of hyperpolarization
2. GAT blockers and GABA-transaminase inhibitors
-more GABA in the synapse for longer, more GABA receptor activation, more hyperpolarization’s and fewer AP’s occurring.
4. GAD modulators
-amp up the activity of the GAD enzyme, less glutamate
5. Prodrug
-increase the precursor for GABA, enhancing bodys ability to make and release GABA

20
Q

GABA can affect what disorder?

A

anxiety

21
Q

Glycine is the…..

A

…..second major inhibitory neurotransmitter in the central nervous system

22
Q

Glycine synthesis and packaging

A

3-phosphoglycerate -> serine -> glycine

  • as long as we are living we can always make glycine, because we have its precursor formed from respiration
  • Packaged into vesicles in the synaptic terminal by VIAAT (same as GABA)
23
Q

Glycine receptor structure

A

-only has a ligand gated ion channel
-Ligand-gated Cl- channel
-pentameric structure, but different subunit composition to GABAa
-common structure involves alpha and beta
We aren’t sure how many binding sites are needed for the glycine receptor to be activated -we don’t know how many interfaces need to be occupied it needs glycine to open

24
Q

differences between GABAa and glycine receptors

A
  • glycine receptors are commonly found both presynaptically and postsynaptically, key difference to GABAa receptor, which is most commonly found post synaptically
  • different pentameric structure
25
Q

Glycine activity termination, reuptake and degradation

A
  1. terminated by high-affinity Na+ dependent glycine re-uptake transporters (GlyTs)
    - Glial cells = GlyT-1
    - Neurons = GlyT-2

once in the cytosol it can be packaged into vesicles by VIAAT

  1. diffusion away from synapse
  2. glycine broken down to serine
26
Q

Hyperekplexia and glycine neurotransmission

A
  • hypertonia (increased muscle tone) and an exaggerated startle response
  • symptoms manifest in relation to unexpected stimuli (loud noises)
  • gene mutations in glycine receptors disrupt normal glycinergic neurotransmission
  • can lead to neuronal hyperexcitability (by impairing glycinergic inhibition)
27
Q

startle goats

A

In startle goats, there is a decreased muscle chloride conductance – can be caused by glycine receptor mutations

  • deficiency in being able to produce inhibition because they don’t have a functional subset of their inhibitory receptors
  • As the goats mature, GABAa receptors are upregulated to compensate

Neuro (21 decks)

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