L-type Ca2+ channel-mediated short-term plasticity of GABAergic synapses (original) (raw)

Nature Neuroscience volume 4, pages 975–976 (2001)Cite this article

Abstract

In the cerebral cortex, the major inhibitory neurotransmitter GABA (γ-aminobutyric acid) is released by GABAergic neurons1 onto GABAA and GABAB 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.

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Acknowledgements

This work was supported by NIH grant NS 30549 and the Coelho Endowment to I.M. K.J. is a Glaxo/Wellcome scholar.

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Authors and Affiliations

  1. Department of Neurology, RNRC 3-131, University of California, Los Angeles School of Medicine, 710 Westwood Plaza, Los Angeles, 90095, California, USA
    Kimmo Jensen & Istvan Mody

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  1. Kimmo Jensen
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  2. Istvan Mody
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Correspondence toIstvan Mody.

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Jensen, K., Mody, I. L-type Ca2+ channel-mediated short-term plasticity of GABAergic synapses.Nat Neurosci 4, 975–976 (2001). https://doi.org/10.1038/nn722

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