GABA: an excitatory transmitter in early postnatal life

E Cherubini, JL Gaiarsa, Y Ben-Ari - Trends in neurosciences, 1991 - cell.com
Trends in neurosciences, 1991cell.com
It inhibits neuronal firing by increasing a Cl-conductance. Bicuculline blocks this effect and
induces interictal discharges. A different picture is present in neonatal hippocampal
neurones, where synaptically released or exogenously applied GABA depolarizes and
excites neuronal membranes-an effect that is due to a different CI-gradient. In fact, dunng the
early neonatal period, GABA acting on GABAA receptors provides most of the excitatory
dr/ve, whereas excitatory glutamatergic synapses are quiescent. It is suggested that during …
It inhibits neuronal firing by increasing a Cl-conductance. Bicuculline blocks this effect and induces interictal discharges. A different picture is present in neonatal hippocampal neurones, where synaptically released or exogenously applied GABA depolarizes and excites neuronal membranes-an effect that is due to a different CI-gradient. In fact, dunng the early neonatal period, GABA acting on GABAA receptors provides most of the excitatory dr/ve, whereas excitatory glutamatergic synapses are quiescent. It is suggested that during development GABA exerts mainly atrophic action through membrane depolarization and a rise in intracellular Ca 2+.
GABA is the major inhibitory transmitter in the adult mammalian CNS. It activates GABAA receptors and inhibits neuronal firing by increasing a CI-conductance, Blockade of GABAA receptors by bicuculline generates epileptic activity. The receptorchannel complex, which has been sequenced, can be allosterically modulated by drugs such as benzodiazepines and barbiturates, known to be therapeutically active in several CNS disorders (eg epilepsy and anxiety)~. In addition to its classical effect on CI-channels, GABA inhibits neuronal activity by activating GABAB receptors coupled to K+ channels 1.
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