Here, we tested the novel hypothesis that 5-HT<sub>2C</sub>R in the BLA drives CRF1 receptor activation to increase CeA neuronal activity in neuropathic pain.
Optogenetic inhibition of mPCF neuronal terminals or local infusion of the CRF receptor 1 (CRFR1) antagonist in the NAc restored the effects of neuropathic pain on morphine-induced CPP behavior, but not in normal mice.