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

行为学研究揭示了终纹床核(BNST)内促肾上腺皮质激素释放因子(CRF)和神经肽Y(NPY)在大鼠疼痛负性情感成分中的相反作用。电生理研究表明，CRF和NPY选择性地作用于BNST II型神经元，并分别激活和抑制这些神经元。组织化学分析表明，BNST向VTA投射的神经元大多为GABA能神经元，并与VTA GABA能神经元突触，提示BNST通过去抑制机制向VTA多巴胺能神经元提供兴奋性驱动。痛诱导的BNST内CRF释放可能激活了BNST的II型神经元，从而抑制了VTA投射的BNST输出神经元，从而减弱了对VTA多巴胺能神经元的兴奋驱动。疼痛诱发的负性情绪可能是由于BNST内VTA多巴胺能神经元通过处理疼痛信息而受到抑制。

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.