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Induction of Depolarization-Induced Suppression of IPSP by Adenosine and Cannabinoids in The Rat Nucleus Accumbens

A short period of depolarization evokes transient suppression of neurotransmitter release (Depolarization-induced Suppression of IPSP: DSI). Recent studies suggest that cannabinoids are candidates for the retrograde messenger required to induce DSI in the hippocampal CA1 area. A G protein-coupled process and inhibition of N-type calcium channels at the presynaptic terminals are believed to be involved in the induction mechanism. We examined DSI induction in the nucleus accumbens in which inputs from multiple sites in the telencephalon, including the hippocampus and basolateral amygdala, converge. Using whole-cell recording from a horizontal slice preparation of nucleus accumbens from the rat brain, we monitored the effect of endogenous cannabinoids on DSI induction and found that 300 nM AM281, a selective cannabinoid CB1 receptor antagonist, resulted in blockade of DSI. Adenosine is reported to suppress neurotransmitter release by inhibiting N-type calcium channels, which is a similar mechanism to that reported for cannabinoid-induced DSI. We therefore examined the effect of endogenous adenosine on DSI induction using DPCPX, a selective A1 receptor antagonist, and found that DSI induction was blocked in the presence of 100 nM DPCPX. These results suggest that cooperative activation of CB1 and A1 receptors contributes to DSI induction in the rat nucleus accumbens.