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Tonic GABAA Receptor–Mediated Signaling in Epilepsy 

Tonic GABAA Receptor–Mediated Signaling in Epilepsy

Chapter:
Tonic GABAA Receptor–Mediated Signaling in Epilepsy
Author(s):

Matthew C. Walker

and Dimitri M. Kullmann

DOI:
10.1093/med/9780199746545.003.0009
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date: 09 July 2017

Fast inhibitory signaling in the brain has conventionally been considered to be predominantly mediated by the vesicular release of GABA from presynaptic terminals onto postsynaptic GABAA receptors.1 Transient opening of such receptors results in a brief increase in postsynaptic permeability to Cl–, generating an inhibitory postsynaptic potential (IPSP) that reduces the probability of firing of the neuron. However, there is abundant evidence that GABA can also act relatively far from its site of release, and this, together with several other discoveries in the last two decades, has contributed to a reappraisal of the roles of GABAA receptors in modulating neuronal and circuit excitability.1

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