The NAc is a critical site of action for reduction of drinking by apremilast.
Recent evidence suggests that increased expression of PDE4 subtypes, namely PDE4b, is linked to human AUD (Next, we sought to determine how acute treatment with apremilast altered functional activity in NAc D1 MSNs and D2 MSNs, which together comprise greater than 90% of the neurons in the NAc and are the 2 major output pathways of this region. We performed ex vivo whole-cell patch clamp electrophysiology in brain slices from male and female hemizygous Dopaminergic neurotransmission in NAc MSNs is largely mediated through PKA signaling, of which PDE4 is a critical regulator. Nishi et al. demonstrated that the PDE4 inhibitor rolipram increased neuronal excitability in isolated MSNs (