Chronic ethanol exposure reversibly inhibits LTP (Durand and Carlen, 1984; Roberto et al., 2002) and dampens LTD in hippocampal neurons (Thinschmidt et al., 2003) (Figure 3J). Indeed, high-dose ethanol treatment can transiently abolish NMDA-dependent LTD in hippocampal neurons and elicit cognitive deficits in rats (Silvestre de Ferron et al., 2015). Impairment of mGluR5-LTD in hippocampal slices following ethanol vapor exposure (Wills et al., 2017) indicates that other types of plasticity may be affected by chronic ethanol. Relevant to the role of plasticity in ethanol-related behaviors, mice susceptible to the development of locomotor sensitization to ethanol show normal hippocampal LTD, whereas mice resistant to ethanol sensitization lack LTD (Coune et al., 2017). We still have an incomplete understanding of how changes in synaptic plasticity are associated with behavioral adaptations produced by chronic ethanol treatment.
