Abstract
RMTg onto DA cells was reduced, and RMTg neurons showed a reduced spontaneous activity in sP rats. In vitro electrophysiology experiments showed that depolarization-induced suppression of inhibition (DSI), a form of endocannabinoid-mediated short term synaptic plasticity expressed by inhibitory synapses from RMTg onto VTA DA neurons, is larger in sP rats. This phenomenon is selectively mediated by the endocannabinoid 2-arachidonoylglycerol (2-AG), which activates presynaptic type 1-cannabinoid (CB1) receptors. The larger DSI in sP rats reflects a difference in the rate 2-AG is degraded, and not in CB1 number and/or function. Given that sP rats are vulnerable phenotypes, and that they express larger DSI, our results suggest that differences in regulation of 2-AG signaling might control specific sources of vulnerability.
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