Reduced Inhibitory Inputs On Basolateral Amygdala Principal Neurons Following Long-Term Alcohol Consumption

Recent studies have shown that manipulating basolateral amygdala (BLA) activity can affect alcohol consumption, particularly following chronic and/or long-term intake. Although the mechanisms underlying these effects remain unclear, the BLA is highly sensitive to emotional stimuli including stress and anxiety. Negative emotional states facilitate alcohol craving and relapse in patients with alcohol use disorders. Consequently, the aim of this study was to determine the effect of long-term (10 weeks) alcohol drinking on synaptic activity in BLA principal neurons. We utilized an intermittent drinking paradigm in rats, which facilitated escalating, binge-like alcohol intake over the 10 week drinking period. We then recorded spontaneous excitatory and inhibitory postsynaptic currents of BLA principal neurons from long-term alcohol drinking rats and aged-matched water drinking controls. Excitatory postsynaptic current properties from long-term alcohol drinking rats were unchanged compared to those from age-matched water drinking controls. Conversely, we observed significant reductions of inhibitory postsynaptic current amplitude and frequency in long-term ethanol drinking rats compared to age-matched water drinking controls. These results highlight substantive decreases in basal inhibitory synaptic activity of BLA principal neurons following long-term alcohol consumption. A loss of inhibitory control in the BLA could explain the high incidence of compulsive drinking and stress- or anxiety-induced relapse in patients with alcohol use disorders.