Evidence exists that cannabinoid receptor type 1 can inhibit voltage-gated calcium channel, decrease intracellular Ca2+ influx, and reduce neurotransmitter release. However, some scholars demonstrated that cannabinoid receptor type 1 can increase extracellular Ca2+ influx and increase neurotransmitter release. Dr. Yi Zhang and his team, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, China used whole cell voltage-clamp and calcium imaging in cultured trigeminal ganglion neurons and found that anandamide directly caused Ca2+ influx, which then triggered an increase of intracellular Ca2+ concentration. Inhibition of voltage-gated calcium channel by anandamide and increase in intracellular Ca2+ concentration by anandamide are two independent events. The underlying mechanisms are similar, both are bidirectional. That is to say, low concentration of anandamide exerts effects by activating cannabinoid receptor type 1 and high concentration of anandamide exerts effects by activating cannabinoid receptor type 1 and vanilloid receptor type 1. The signaling pathways involved in two independent events are different. Protein kinase C signaling pathway is involved in anandamide inhibition of voltage-gated calcium channel, but it does not participate in the process during which anandamide increases intracellular Ca2+ concentration. These findings provide evidence for studying the mechanism underlying the neural excitatory effects of anandamide. Related results were published in Neural Regeneration Research (Vol. 9, No. 8, 2014).
Source: Neural Regeneration Research