2014 Apr 15;9(8):878-87. doi: 10.4103/1673-5374.131607.
Regulatory effects of anandamide on intracellular Ca(2+) concentration increase in trigeminal ganglion neurons.
Abstract
Activation of cannabinoid receptor type 1 on presynaptic neurons is postulated to suppress neurotransmission by decreasing Ca(2+) influx through high voltage-gated Ca(2+) channels. However, recent studies suggest that cannabinoids which activate cannabinoidreceptor type 1 can increase neurotransmitter release by enhancing Ca(2+) influx in vitro. The aim of the present study was to investigate the modulation of intracellular Ca(2+) concentration by the cannabinoid receptor type 1 agonist anandamide, and its underlying mechanisms. Using whole cell voltage-clamp and calcium imaging in cultured trigeminal ganglion neurons, we found that anandamide directly caused Ca(2+) influx in a dose-dependent manner, which then triggered an increase of intracellular Ca(2+) concentration. The cyclic adenosine and guanosine monophosphate-dependent protein kinase systems, but not the protein kinase C system, were involved in the increased intracellular Ca(2+) concentration by anandamide. This result showed that anandamide increased intracellular Ca(2+) concentration and inhibited high voltage-gated Ca(2+) channels through different signal transduction pathways.
KEYWORDS:
NIH grant; anandamide; calcium; cannabinoid receptor type 1; cyclic adenosine monophosphate protein kinase; endocannabinoids; nerve regeneration; neural regeneration; neurons; patch-clamp technique; protein kinase C; trigeminal ganglion; vanilloid receptor; voltage-dependent calcium channels
- PMID:
- 25206906
- [PubMed]
