Abstract
Several lines of evidence suggest that the modulation of presynaptic GABA release is mediated by a variety of receptors including; presynaptic AMPA, cannabinoid, GABAB, 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.
Highlights
Inhibition is essential in shaping response properties in single cells and assisting co-operativtity in large populations of cells
Previous studies have suggested that glutamate is released from postsynaptic dendrites as a result of depolarisation induced suppression of inhibition (DSI) acting as a retrograde messenger [6, 100].This glutamate activates presynaptic kainate receptors that probably inactivate presynaptic calcium channels, a reduced influx of calcium decreasing GABA release [49, 60, 78]
Observation was extended to CA1, where GABA release at CCK-positive basket cells targeting pyramidal cells was decreased via presynaptic cannabinoid receptor type-1 (CB1) receptors at low frequencies of presynaptic firing, the presynaptic basket cell recovered from this inhibition of GABA release when it was activated at higher firing frequencies [27]
Summary
Inhibition is essential in shaping response properties in single cells and assisting co-operativtity in large populations of cells. Selective insertion of presynaptic receptors such as kainate, cannabinoid (CB), AMPA, NMDA, GABAB, opioid, and metabotropic glutamate receptors (mGluRs) may add further diversity to interneuronal function. These signalling pathways exert a modulatory role on transmitter release at inhibitory synapses, though how all these receptors/modulators variously regulate inhibition in a cell type-specific manner still requires detailed investigation. I will be reviewing these two subclasses of basket cells, and dendrite targeting cells that express CCK and focus on presynaptic modulation via kainate and cannabinoid receptors with some discussion on opioid receptors
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