Tonic endocannabinoid-mediated modulation of GABA release is independent of the CB1 content of axon terminals

Nora Lenkey, Tekla Kirizs, Noemi Holderith, Zoltán Máté, Gábor Szabó, E. Sylvester Vizi, Norbert Hájos and Zoltan Nusser ()
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Nora Lenkey: Lendület Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences
Tekla Kirizs: Lendület Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences
Noemi Holderith: Lendület Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences
Zoltán Máté: Institute of Experimental Medicine, Hungarian Academy of Sciences
Gábor Szabó: Institute of Experimental Medicine, Hungarian Academy of Sciences
E. Sylvester Vizi: Laboratory of Drug Research, Institute of Experimental Medicine, Hungarian Academy of Sciences
Norbert Hájos: Lendület Laboratory of Network Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences
Zoltan Nusser: Lendület Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: Abstract The release of GABA from cholecystokinin-containing interneurons is modulated by type-1 cannabinoid receptors (CB1). Here we tested the hypothesis that the strength of CB1-mediated modulation of GABA release is related to the CB1 content of axon terminals. Basket cell boutons have on average 78% higher CB1 content than those of dendritic-layer-innervating (DLI) cells, a consequence of larger bouton surface and higher CB1 density. The CB1 antagonist AM251 caused a 54% increase in action potential-evoked [Ca2+] in boutons of basket cells, but not in DLI cells. However, the effect of AM251 did not correlate with CB1 immunoreactivity of individual boutons. Moreover, a CB1 agonist decreased [Ca2+] in a cell type- and CB1-content-independent manner. Replica immunogold labelling demonstrated the colocalization of CB1 with the Cav2.2 Ca2+ channel subunit. Our data suggest that only a subpopulation of CB1s, within nanometre distances from their target Cav2.2 channels, are responsible for endocannabinoid-mediated modulation of GABA release.

Date: 2015
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DOI: 10.1038/ncomms7557

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