Induction Of Depolarized-induced Suppression Of IPSC By Adenosine And Cannabinoid In The Rat Nucleus Accumbens

Depolarization-induced suppression of IPSP (DSI) is reported at first and its mechanism is well investigated at the rat hippocampus. The short period of depolarization evokes transient suppression of neurotransmitter release, which process requires the retrograde signals. Recent studies suggested that cannabinoid is the candidate for the retrograde messenger in the hippocampal CA1 area. The precise mechanism underlying DSI induced by cannabinoid is currently unknown, however, G protein-coupled process and the inhibition of N-type calcium channels at the presynaptic terminals are believed to be involved in the induction mechanism. We examined the induction of DSI in the nucleus accumbens, which is supposed to have a gating mechanism against the input from the hippocampus and amygdale and the converged information is transferred to the motor function of the brain. We made a horizontal slice preparation of nucleus accumbens from the rat brain and the effect of endogenous cannabinoid on the induction of DSI was monitored using the whole cell recording in the presence of 300 nM AM251, an selective CB1 receptor antagonist, resulted in the blockade of DSI. On the other hand, adenosine has been reported to suppress the neurotransmitter release by inhibiting N-type calcium channels, which is the similar mechanism as is reported in DSI evoked by cannabinoid. We examined the effect of endogenous adenosine on DSI induction by using DPCPX, a selective A1 receptor antagonist. DSI induction was blocked in the presence of 100 nM DPCPX. These results suggested that cooperative activation of CB1 and A1 receptors contributes to DSI induction mechanism in the rat nucleus accumbens.