mice lacking TRPV1, these mice exhibited an enhanced locomotor response to cocaine that was maintained as behavioral sensitization developed with repeated daily administration of cocaine (Grueter et al., 2010). Assuming that the absence of TRPV1 specifically in NAc indirect pathway MSNs was responsible for the enhanced cocaine-induced locomotor activity, the LTD triggered by TRPV1 may function as a brake on cocaine-elicited locomotor activity. This role is opposite to that proposed for NMDAR-dependent LTD. However, since the TRPV1-dependent LTD is restricted to indirect pathway MSNs while NMDAR-dependent LTD occurs in both subtypes of MSNs, it is not unexpected that these forms of synaptic plasticity may have different behavioral roles.
