et al. 1992, Gerdeman, Ronesi et al. 2002, Adermark, Talani et al. 2009, Mathur, Capik et al. 2011). The glutamatergic synapses that express LTD are made by afferents from the cortex, as these inputs, but not thalamic inputs, contain CB1 receptors (Wu, Kim et al. 2015). Acute ethanol exposure appears to enhance this form of LTD while inhibiting LTP in the DMS (Yin, Park et al. 2007). Chronic exposure to ethanol prevents the induction of this LTD in the DLS when examined in an ex vivo brain slice preparation (Xia, Li et al. 2006, Adermark, Talani et al. 2009, DePoy, Daut et al. 2013). This loss of LTD is observed with both passive ethanol exposure and after voluntary ethanol consumption in rat and mouse. It is not yet clear if the loss of LTD is due to a general impairment of CB1 signaling, occlusion of LTD by presynaptic depression induced by the in vivo ethanol exposure, or interference with some other signaling event involved in LTD induction. The inhibitory effect of a CB1 agonist is lost following chronic ethanol consumption (Adermark et al., 2011), indicating that CB1 activity or a downstream mechanism is impaired. A few days abstinence following chronic
