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Parabrachial Calcitonin Gene-Related Peptide Neurons Mediate Conditioned Taste Aversion

机译:臂旁降钙素基因相关肽神经元介导条件性味觉厌恶

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摘要

Conditioned taste aversion (CTA) is a phenomenon in which an individual forms an association between a novel tastant and toxin-induced gastrointestinal malaise. Previous studies showed that the parabrachial nucleus (PBN) contains neurons that are necessary for the acquisition of CTA, but the specific neuronal populations involved are unknown. Previously, we identified calcitonin gene-related peptide (CGRP)-expressing neurons in the external lateral subdivision of the PBN (PBel) as being sufficient to suppress appetite and necessary for the anorexigenic effects of appetite-suppressing substances including lithium chloride (LiCl), a compound often used to induce CTA. Here, we test the hypothesis that PBel CGRP neurons are sufficient and necessary for CTA acquisition in mice. We show that optogenetic activation of these neurons is sufficient to induce CTA in the absence of anorexigenic substances, whereas genetically induced silencing of these neurons attenuates acquisition of CTA upon exposure to LiCl. Together, these results demonstrate that PBel CGRP neurons mediate a gastrointestinal distress signal required to establish CTA.
机译:有条件的口感厌恶(CTA)是一种现象,其中个体在新型味觉与毒素诱导的胃肠不适之间形成联系。先前的研究表明,臂旁旁核(PBN)包含获得CTA所必需的神经元,但所涉及的特定神经元群体尚不清楚。先前,我们确定PBN(PBel)外侧外侧细分中表达降钙素基因相关肽(CGRP)的神经元足以抑制食欲,并且对于抑制食欲的物质(包括氯化锂(LiCl))具有厌食作用,通常用于诱导CTA的化合物。在这里,我们测试PBel CGRP神经元是小鼠CTA采集的充分和必要的假设。我们显示这些神经元的光遗传学激活足以在没有厌食症物质的情况下诱导CTA,而这些神经元的遗传诱导沉默在暴露于LiCl后会减弱CTA的获得。总之,这些结果表明,PBel CGRP神经元介导建立CTA所需的胃肠道不适信号。

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