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Curr Neuropharmacol. 2009 Jun;7(2):125-31. doi: 10.2174/157015909788848875.

Presynaptic cell dependent modulation of inhibition in cortical regions.

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  • 1University of London, School of Pharmacy, Department of Pharmacology 29/39 Brunswick Square, London WC1N 1AX, UK.


Several lines of evidence suggest that the modulation of presynaptic GABA release is mediated by a variety of receptors including; presynaptic AMPA, cannabinoid, GABA(B), kainate, metabotropic glutamate, NMDA, and opioid receptors. The evidence supporting presynaptic modulation of inhibition is predominantly obtained from studying stimulus elicited, spontaneous or miniature synaptic events, where the information regarding the identity of the presynaptic cell is lost. This article summarises these findings then focuses on another approach to study the presynaptic modulation of GABA release by comparing the modulation of GABA release at unitary synapses identified morphologically, immunocytochemically and electrophysiologically. To date, evidence for cell-type specific regulation of presynaptic inhibition at identified synapses involving most of the above presynaptic receptors does not exist. Therefore, the key presynaptic modulators that will be focused on here are kainate and cannabinoid receptors and their intracellular signalling cascades that orchestrate GABA release. There will be some discussion on presynaptic modulation via opioid receptors at identified synapses. This review provides evidence to suggest a cell-type specific modulation of presynaptic inhibition in cortical regions.


GABAA; Presynaptic; cannabinoid receptor type-1 (CB1); cortical; depolarisation induced suppression of inhibition (DSI).; inhibition; kainate receptors; mGluRs

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