Ethanol Experience Enhances Glutamatergic Ventral Hippocampal Inputs to D1 Receptor-Expressing Medium Spiny Neurons in the Nucleus Accumbens Shell.

摘要: A growing number of studies implicate alterations in glutamatergic signaling within the reward circuitry brain during alcohol abuse and dependence. key integrator circuit is nucleus accumbens, more specifically, dopamine D1 receptor-expressing medium spiny neurons (D1-MSNs) this region, which have been implicated formation dependence to many drugs including alcohol. D1-MSNs receive input from several regions; however, it not currently known how individual inputs onto are altered by experience. Here, we investigate input-specific adaptations transmission response varying levels Virally mediated expression Channelrhodopsin ventral hippocampal (vHipp) glutamate male mice allowed for selective activation vHipp D1-MSN synapses. Therefore, were able compare synaptic low high experience vitro vivo Alcohol enhanced activity abolished LTD at Following chronic experience, GluA2-lacking AMPARs, Ca permeable, inserted into These findings support reversal alcohol-induced insertion Ca-permeable AMPARs enhancement as potential targets intervention early exposure alcohol.SIGNIFICANCE STATEMENT Given roles accumbens (NAc) integrating cortical allocortical information learning, vital understand region such The strength excitatory hippocampus NAc has positively associated with reward-related behaviors, but unclear whether or ethanol affects these inputs. Here show that vHipp-NAc synapses indeed exposure, being following This work provides insight ethanol-induced suggests that, similarly cocaine, strengthening promotes behavior.