Huntington’s disease (HD) is an inherited neurodegenerative disorder caused by a polyglutamine (CAG) expansion in the huntingtin gene. Striatal and cortical dysfunction are the hallmark neuropathological features underlying dyskinesia (e.g., chorea) and akinesia at later stages. However, prominent psychiatric symptoms manifest prior to motor dysfunction. We have recently shown in the Q175 mouse model of HD that suppressed motivation – one of the earliest indicators of HD – is associated with compromised dopaminergic signaling and network dynamics in the nucleus accumbens (NAc). We will discuss how pharmacological elevation of endocannabinoid levels in Q175 mice rescues compromised neurobiological markers and ameliorates motivational deficits. Our findings indicate that modulating NAc abnormalities with endocannabinoid-based therapies may be beneficial in treating the prodromal psychiatric deficits of HD.