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

Author

Listed:
  • 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
    János Szentágothai School of Neurosciences, Semmelweis University)

  • 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)

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.

Suggested Citation

  • Nora Lenkey & Tekla Kirizs & Noemi Holderith & Zoltán Máté & Gábor Szabó & E. Sylvester Vizi & Norbert Hájos & Zoltan Nusser, 2015. "Tonic endocannabinoid-mediated modulation of GABA release is independent of the CB1 content of axon terminals," Nature Communications, Nature, vol. 6(1), pages 1-15, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7557
    DOI: 10.1038/ncomms7557
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