L-type Ca²⁺ channel-mediated short-term plasticity of GABAergic synapses

Abstract

In the cerebral cortex, the major inhibitory neurotransmitter GABA (γ-aminobutyric acid) is released by GABAergic neurons¹ onto GABA_A and GABA_B receptors, and regulates neuronal excitability, postsynaptic action potential firing, and dendritic and synaptic integration². Various interneurons use either N- or P/Q-type Ca²⁺ channels for the Ca²⁺ influx into their terminals³, whereas L-type Ca²⁺ channels are not normally associated with GABA release. In dual recordings from hippocampal basket cells and granule cells, we now report that short-term plasticity of GABA release is controlled by L-type Ca²⁺ channels at presynaptic firing rates in the gamma-frequency (40 Hz) range⁴; at these GABAergic synapses, L-type Ca²⁺ channel antagonists converted post-tetanic potentiation into depression, identifying L-type Ca²⁺ channels as important modulators of plasticity at GABAergic synapses.