While the transient receptor potential vanilloid 1 (TRPV1) ion channel, a non-selective calcium-permeable cation channel with high Ca 2+ permeability, mainly integrates physical and chemical stimuli for nociception, recent studies suggest that it has a role beyond a noxious thermal sensor. In fact, TRPV1 is presently being considered as a target for treating pathophysiological processes including pain, fear, and anxiety disorders. Although this ion channel has many potential roles, its underlying mechanism of action remains elusive. Here we show in mice that activation of TRPV1-, by the exogenous agonist capsaicin-, regulates synaptic activity in both glutamatergic and GABAergic synaptic transmission. Moreover, activation by the endogenous activator N-arachidonoyl taurine (NAT), induced similar effects as capsaicin. On the other hand, taurine, the decomposition product of NAT, strongly depressed the evoked glutamatergic synaptic transmission. In addition to these findings, we also show the immunohistochemical distribution of TRPV1 in the prefrontal cortex (PFC) of mice, as such studies are currently less frequent in the PFC. Overall, these observations allow for a better understanding of how TRPV1 helps regulate excitatory and inhibitory synaptic activity in the PFC of mice.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.