The origin of glutamatergic synaptic inputs controls synaptic plasticity and its modulation by alcohol in mice nucleus accumbens.

摘要: It is widely accepted that long-lasting changes of synaptic strength in the nucleus accumbens (NAc), a brain region involved drug reward, mediate acute and chronic effects alcohol. However, our understanding mechanisms underlying alcohol on plasticity limited by fact NAc receives glutamatergic inputs from distinct regions (e.g., prefrontal cortex (PFCx), amygdala hippocampus), each providing different information spatial, emotional cognitive). Combining whole-cell patch-clamp recordings optogenetic technique, we examined plasticity, its regulation alcohol, at cortical, hippocampal fresh slices mouse tissue. We showed origin determines basic properties transmission, expression spike-timing dependent long-term depression (tLTD) potentiation (LTP) (tLTP) their While observed both tLTP tLTD amygadala synapses, cortical only undergo tLTD. Functionally, provide evidence Ethyl Alcohol (EtOH) has little higher order coming PFCx, while severely impacting ability contextual to induce strength.