Other forms of LTD observed in hippocampus and elsewhere involve activation of mGluRs (reviewed in Lüscher and Huber 2010). One report indicates that EtOH, at concentrations associated with severe intoxication, prevents mGluR-LTD at hippocampal synapses (Overstreet et al. 1997). At glutamatergic synapses onto cerebellar Purkinje neurons mGluR-LTD involves decreased surface expression and function of AMPARs (Ito 2001). Acute EtOH exposure inhibits this cerebellar LTD (Belmeguenai et al. 2008; Su et al. 2010), most likely due to inhibition of voltage-gated calcium channels and mGluR function. This finding is intriguing given that acute EtOH is known to impair motor coordination, and cerebellar function has been implicated in these effects. In the dorsal striatum, LTD involving these receptors also requires endocannabinoid (EC) signaling from the post to the presynaptic neuron (retrograde EC signaling) and subsequent activation of CB1 cannabinoid receptors (Gerdeman et al. 2002). The expression of this form of LTD appears to be on the presynaptic side of the synapse. Acute EtOH increases the expression of this EC-dependent mGluR-LTD in dorsal striatum (Yin et al. 2007). It is presently not clear what mechanisms contribute to this effect of EtOH.
