Channelpedia

PubMed 25843413


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Slo1 , TRP , TRPV , TRPV1



Title: The interactive role of cannabinoid and vanilloid systems in hippocampal synaptic plasticity in rats.

Authors: Lida Tahmasebi, Alireza Komaki, Ruhollah Karamian, Siamak Shahidi, Abdolrahman Sarihi, Iraj Salehi, Ali Nikkhah

Journal, date & volume: Eur. J. Pharmacol., 2015 Jun 15 , 757, 68-73

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25843413


Abstract
Long-term potentiation (LTP) has been most thoroughly studied in the hippocampus, which has a key role in learning and memory. Endocannabinoids are one of the endogenous systems that modulate this kind of synaptic plasticity. The activation of the vanillioid system has also been shown to mediate synaptic plasticity in the hippocampus. In addition, immunohistochemical studies have shown that cannabinoid receptor type 1 (CB1) and vanilloid receptor 1 (TRPV1) are closely located in the hippocampus. In this study, we examined the hippocampal effects of co-administrating WIN55-212-2 and capsaicin, which are CB1 and TRPV1 agonists, respectively, on the induction of LTP in the dentate gyrus (DG) of rats. LTP in the hippocampal area was induced by high-frequency stimulation (HFS). Our results indicated that the cannabinoid agonist reduced both field excitatory post-synaptic potential (fEPSP) slope and population spike (PS) amplitude after HFS with respect to the control group, whereas the vanilloid agonist increased these parameters along with the increased induction of LTP as compared to the control group. We also showed that the co-administration of cannabinoid and vanilloid agonists had different effects on fEPSP slope and PS amplitude. It seems that agonists of the vanilloid system modulate cannabinoid outputs that cause an increase in synaptic plastisity, while in contemporary consumption of two agonist, TRPV1 agonist can change production of endocannabinoid, which in turn result to enhancement of LTP induction. These findings suggest that the two systems may interact or share certain common signaling pathways in the hippocampus.