GABAergic Synapse

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Chemical synapses can be classified according to the neurotransmitter that the presynaptic neuron is utilizing. GABAergic presynaptic axon terminals release Gamma aminobutyric acid​, which acts on postsynaptic GABAA receptors, opening an intrinsic chloride channel. This action usually inhibits the postsynaptic neuron by hyperpolarizing the cell membrane.[16]


Neurons​ are incapable of de novo synthesis of Glutamate​ or Gamma aminobutyric acid[2]​. Instead, they take up glutamine released from Astrocytes​, which is then converted to glutamate by Glutaminase​. GABAergic neurons and their axon terminals can be identified by visualising Glutamic acid decarboxylase​. This enzyme catalyses the subsequent Decarboxylation​ of glutamate to GABA. GABA is then taken up into Synaptic vesicles​ by the Vesicular GABA transporter​ (VGAT). Action potentials invading the axon terminal trigger the release machinery, causing synaptic GABA concentration to rise transiently to millimolar concentrations[4]​. Released GABA is rapidly cleared by GABA transporters​ (GAT 1 to 3)[5][6]​, of which GAT1 is mainly expressed presynaptically, and GAT3 on astrocytes[7][8]​. GAT1 and GAT3 can also operate in reverse mode and thus regulate GABAergic tone[9]​.

Main components

The presynaptic terminal of a GABAergic neuron takes up Glutamine​ released from neighbouring astrocytes, where it was converted from glutamate by Glutamate synthetase​. Glutamine is then metabolised into Gamma aminobutyric acid​ through Glutaminase​ and Glutamic acid decarboxylase​ (GAD). The Vesicular GABA transporter​ (VGAT) translocates GABA into synaptic vesicles, from where it is released into the Synaptic cleft​. Here, GABA can act on synaptic GABAA receptors​ or MetabotropicGABAB receptors​, and can also diffuse away to reach peri- and extrasynaptic GABAA receptors. GABA reuptake is mediated mainly by the transporters GAT1 on presynaptic terminals and GAT3 on astrocytes.

Within astrocytes, degradation of GABA is catalysed by GABA transaminase​ to succinate semialdehyde (SSA), and further by SSA dehydrogenase to Succinic acid​, which is fed into the Tricarboxylic acid cycle[2]​. Synaptic GABAA receptors bind to the scaffolding protein Gephyrin​, but can also diffuse out of synaptic sites, where exo-/endocytosis takes place.

Comparison to excitatory synapses

Basic numbers on GABAergic transmission are most readily available for the Hippocampus​. In this region, about 15-20 % of all neurons use GABA as their main neurotransmitter[12][13]​. Similarly, the majority of hippocampal synapses are glutamatergic and the relative number of inhibitory synapses remains low: Pyramidal neurons​ and Basket cells​ receive about 6 % inhibitory versus 94 % excitatory inputs, while other interneuron types can have 20-30 % inhibitory inputs[14][15]​. Because of architectonic similarities, these estimates are likely to be in the same range also for the cortex[16][17]​. Two factors help explain why, despite these numbers, excitation and inhibition can still be at balance in the brain, allowing network operations to be under interneuron control: (i) several types of interneurons including basket and chandelier cells are characterised by considerably faster spiking rates when compared to principal neurons (in the order of 15 Hz versus 1 Hz [13]​, and (ii) tonic inhibition mediated by extrasynaptic GABAARs is quantitatively important, with a three to four times larger total charge transfer compared to synaptic inhibition [18][6][19]​.

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Created: 2018-01-14T21:40:15.906Z
Last Modified: 2018-01-19T01:07:14.612Z