Ethanol can also affect striatal plasticity (Lovinger and Kash, 2015). For example, acute ethanol application blocks LTP (Figure 2U) and has diverse effects on LTD (Clarke and Adermark, 2010; McCool, 2011; Yin et al., 2007). In contrast, chronic ethanol facilitates corticostriatal LTP (Wang et al., 2012; Xia et al., 2006) (Figure 3M) and impairs endocannabinoid-mediated disinhibition in the dorsolateral striatum (Adermark et al., 2011c). Furthermore, chronic ethanol dampens striatal LTD at excitatory synapses (Adermark et al., 2011c; Cui et al., 2011; DePoy et al., 2013) (Figure 3N). With novel optogenetic and transgenic tools, scientists can now study pathway-specific ethanol effects. For example, excessive ethanol intake potentiates AMPA- and NMDA-mediated transmission at the medial prefrontal cortex (mPFC) input and increases glutamate release from BLA afferents to the dorsomedial striatum (DMS). These changes could explain the effect of chronic ethanol exposure on striatal LTP, as paired activation of the mPFC and BLA inputs induces robust LTP of the corticostriatal input to the DMS (Ma et al., 2017).
