Intracellular calcium concentration rises have been reported following activation of GABA(A) receptors in neonatal preparations and attributed to activation of voltage-dependent Ca2+ channels. However, we show that, in cerebellar interneurons, GABA(A) agonists induce a somatodendritic Ca2+ rise that persists at least until postnatal day 20 and is not mediated by depolarization-induced Ca2+ entry. A local Ca2+ elevation can likewise be elicited by repetitive stimulation of presynaptic GABAergic afferent fibers. We find that, following GABA(A) receptor activation, bicarbonate-induced Cl- entry leads to cell depolarization, Cl- accumulation, and osmotic tension. We propose that this tension induces the intracellular Ca2+ rise as part of a regulatory volume decrease reaction. This mechanism introduces an unexpected link between activation of GABA(A) receptors and intracellular Call elevation, which could contribute to activity-driven synaptic plasticity.
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