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GABAergic

Synaptic transmissin

QuestionAnswer
GABAergic synapse 1. Synthesis 2. Storage 3. Metabolism - uptake and breakdown 4. Action - GABA receptors
GABA synthesis From glutamate via glutamic acid decarboxylase (GAD) in cytosol.
GAD Two forms: 67 and 65 preferentially located in nerve terminal 67: constitutively active saturated with PLP 65: apoenzyme with no PLP bound
GABA synthesis - drugs 1. Hydrazides - react with PLP (i.e. eliminate) 2. ATP - inhibits activation of GAD by PLP 3. iP - promotes activation of GAD by PLP 4. Glu competitive inhibitors, e.g. allylglycine
GABA storage From cytosol to vesicle via VGAT, proton driven transport.
GABA metabolism 1. Uptake by GABA uptake T (GAT) - glial and neuronal 2. Breakdown by GABA transaminase (GABA-T) in mitochondria
GABA metabolism - drugs 1. glial GAT inhibitor: B-alanine 2. neuronal GAT inhibitor: ACHC
GABAergic synapse 1. Synthesis 2. Storage 3. Metabolism - uptake and breakdown 4. Action - GABA receptors
GABA synthesis From glutamate via glutamic acid decarboxylase (GAD) in cytosol.
GAD Two forms: 67 and 65 preferentially located in nerve terminal 67: constitutively active saturated with PLP 65: apoenzyme with no PLP bound
GABA synthesis - drugs 1. Hydrazides - react with PLP (i.e. eliminate) 2. ATP - inhibits activation of GAD by PLP 3. iP - promotes activation of GAD by PLP 4. Glu competitive inhibitors, e.g. allylglycine
GABA storage From cytosol to vesicle via VGAT, proton driven transport.
GABA metabolism 1. Uptake by GABA uptake T (GAT) - glial and neuronal 2. Breakdown by GABA transaminase (GABA-T) in mitochondria
GABA metabolism - drugs 1. glial GAT inhibitor: B-alanine 2. neuronal GAT inhibitor: ACHC 3. GABA-T inhibitor: sodium valproate and gamma-vinyl GABA (anticonvulsant)
GABA actions - GABA receptors 1. GABAa - ionotropic (- bicuculline) 2. GABAb - metabotopic, baclofen (-2-OH-saclofen)
GABAa actions - primary mediators of fast inhibitory synaptic transmission in the CNS, e.g. modify spike timing - permit chloride and bicarbonate ions - hyperpolarising or increasing cell conductance - depolarising in immature neurons
GABAa R modulation sites 1. Benzodazepine 2. Barbiturate 3. Anaesthetics - volatile and intravenous 4. Picrotoxin 5. Steroid 6. GABA
GABAa R structure - Cyc-loop superfamily - Pentameric ligand-gated channel - 4 membrane spanning regions (M1-M4) - M2 form pores
GABAa 7 subunits - subunit composition determines the functional properties and localisation (phasic and tonic) 1) GABA affinity 2) activation and deactivation kinetics (duration of conductance change) 3) onset and recovery from desensitisation 4) single channel conductance (magnitude of conductance change)
GABA subunits e.g. A1B2Y2 (major: anticonvulsant and sedative actions of BZDs) e.g. A2B3Y2 (minor: anxiolytic action of BZDs) A and B form functional receptors +Y is required for BZD pharmacology A determines the type D associates with A4 and A6 : high affinity with (-)BZD E related to Y, with ABY form insensitive to BZD Pie related to B, (-)steroid Theta to B1, (-)GABA
GABAa receptor composition (A1-6) (B1-3) (Y1-3) and others 2A and 2B subunits and a fifth subunit belongs to any of the other classes
GABAa - phasic inhibition - in synaptic cleft, producing IPSCs - IPSC shape: activated rapidly, decayed slowly, and biphasically depending on intrinsic properties of GABAa-R (subunits)
GABAa - tonic inhibition - non-synaptic communication (extrasynaptic) - spillover neurotransmitters (ambient GABA) - mostly ABD composition (Delta subunit), ideal for low concentration for sustained time period
Created by: JonLai
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