Tags

Type your tag names separated by a space and hit enter

Cannabidiol-induced intracellular Ca2+ elevations in hippocampal cells.
Neuropharmacology 2006; 50(5):621-31N

Abstract

The phytocannabinoid cannabidiol (CBD) is at the forefront of therapeutic cannabinoid research due to its non-psychotropic properties. Research supports its use in a variety of disorders, yet the cellular mechanisms of its action remain unclear. In this study, the effect of CBD upon Ca2+ homeostasis in hippocampal cells was characterised. CBD (1 microM) elevated intracellular Ca2+ ([Ca2+]i) by approximately +45% of basal Ca2+ levels in both glia (77% responders) and neurones (51% responders). Responses to CBD were reduced in high excitability HEPES buffered solution (HBS), but not affected in low excitability/low Ca2+ HBS. CBD responses were also significantly reduced (by 50%) by the universal Ca2+ channel blocker cadmium (50 microM) and the L-type specific Ca2+ channel blocker nifedipine (20 microM). Interestingly, intracellular store depletion with thapsigargin (2 microM) had the most dramatic effect on CBD responses, leading on average to a full block of the response. Elevated CBD-induced [Ca2+]i responses (>+100%) were observed in the presence of the CB1 receptor antagonist, AM281 (1 microM), and the vanilloid receptor antagonist, capsazepine (CPZ, 1 microM). Overall, our data suggest that CBD modulates hippocampal [Ca2+]i homeostasis via intracellular Ca2+ stores and L-type VGCC-mediated Ca2+ entry, with tonic cannabinoid and vanilloid receptor signalling being negatively coupled to this pathway.

Authors+Show Affiliations

School of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16386766

Citation

Drysdale, Alison J., et al. "Cannabidiol-induced Intracellular Ca2+ Elevations in Hippocampal Cells." Neuropharmacology, vol. 50, no. 5, 2006, pp. 621-31.
Drysdale AJ, Ryan D, Pertwee RG, et al. Cannabidiol-induced intracellular Ca2+ elevations in hippocampal cells. Neuropharmacology. 2006;50(5):621-31.
Drysdale, A. J., Ryan, D., Pertwee, R. G., & Platt, B. (2006). Cannabidiol-induced intracellular Ca2+ elevations in hippocampal cells. Neuropharmacology, 50(5), pp. 621-31.
Drysdale AJ, et al. Cannabidiol-induced Intracellular Ca2+ Elevations in Hippocampal Cells. Neuropharmacology. 2006;50(5):621-31. PubMed PMID: 16386766.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cannabidiol-induced intracellular Ca2+ elevations in hippocampal cells. AU - Drysdale,Alison J, AU - Ryan,Duncan, AU - Pertwee,Roger G, AU - Platt,Bettina, Y1 - 2005/12/28/ PY - 2005/10/07/received PY - 2005/11/09/revised PY - 2005/11/15/accepted PY - 2006/1/3/pubmed PY - 2006/7/11/medline PY - 2006/1/3/entrez SP - 621 EP - 31 JF - Neuropharmacology JO - Neuropharmacology VL - 50 IS - 5 N2 - The phytocannabinoid cannabidiol (CBD) is at the forefront of therapeutic cannabinoid research due to its non-psychotropic properties. Research supports its use in a variety of disorders, yet the cellular mechanisms of its action remain unclear. In this study, the effect of CBD upon Ca2+ homeostasis in hippocampal cells was characterised. CBD (1 microM) elevated intracellular Ca2+ ([Ca2+]i) by approximately +45% of basal Ca2+ levels in both glia (77% responders) and neurones (51% responders). Responses to CBD were reduced in high excitability HEPES buffered solution (HBS), but not affected in low excitability/low Ca2+ HBS. CBD responses were also significantly reduced (by 50%) by the universal Ca2+ channel blocker cadmium (50 microM) and the L-type specific Ca2+ channel blocker nifedipine (20 microM). Interestingly, intracellular store depletion with thapsigargin (2 microM) had the most dramatic effect on CBD responses, leading on average to a full block of the response. Elevated CBD-induced [Ca2+]i responses (>+100%) were observed in the presence of the CB1 receptor antagonist, AM281 (1 microM), and the vanilloid receptor antagonist, capsazepine (CPZ, 1 microM). Overall, our data suggest that CBD modulates hippocampal [Ca2+]i homeostasis via intracellular Ca2+ stores and L-type VGCC-mediated Ca2+ entry, with tonic cannabinoid and vanilloid receptor signalling being negatively coupled to this pathway. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/16386766/Cannabidiol_induced_intracellular_Ca2+_elevations_in_hippocampal_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(05)00394-1 DB - PRIME DP - Unbound Medicine ER -