Neurons within the GPe are inhibited during acute ethanol exposure (Criswell, Simson et al. 1995, Abrahao, Chancey et al. 2016). A recent study has described ethanol inhibition of the activity of a subset of neurons in the GPe. This inhibitory effect is observed at ethanol concentrations associated with mild intoxication (e.g. 10 mM). The ethanol sensitive GPe neurons exhibit firing rates in the low frequency range, and are characterized by the expression of the transcription factors NPAS1 and Lhx6 (Abrahao, Chancey et al. 2016). The mechanism underlying this inhibitory ethanol action appears to be potentiation of the function of large-conductance (BK) potassium channels, a well-known target for acute ethanol actions (Dopico, Bukiya et al. 2014). In vivo, ethanol administration also inhibited firing in neurons with low baseline firing rates in the GPe of awake, freely-moving mice (Abrahao, Chancey et al. 2016). Interestingly, GPe neurons that project back to striatum (the “arkypallidal” neurons) appear to be among those inhibited by ethanol. Thus, ethanol can mediate disinhibition of striatum via suppression of the inhibitory arkypallidal input to the striatum, in addition to ethanol effects on intrastriatal synaptic connections.
