Study on neuronal mechanisms for negative emotion using behavioral and optogenetical analyses

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Behavioral studies revealed the opposing roles of corticotropin-releasing factor (CRF) and neuropeptide Y (NPY) within the bed nucleus of the stria terminalis (BNST) in the negative affective component of pain in rats. Electrophysiological studies demonstrated that CRF and NPY selectively act on BNST type II neurons, and activates and suppresses these neurons, respectively. Histochemical analyses showed that most of BNST output neurons projecting to the VTA are GABAergic neurons, which synapse onto VTA GABAergic neurons, suggesting the excitatory drive from the BNST to the VTA dopaminergic neurons via a disinhibition mechanism. Pain-induced release of CRF within the BNST may activate BNST type II neurons, which could suppress VTA-projecting BNST output neurons, thereby attenuating the excitatory drive to the VTA dopaminergic neurons. Pain-induced negative emotion may be due to the suppression of VTA dopaminergic neurons via the processing of pain information in the BNST.