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Homeostatic circuits selectively gate food cue responses in insular cortex

机译：稳态电路选择性地控制岛皮层中的食物提示反应

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摘要

Physiological needs bias perception and attention to relevant sensory cues. This process is 'hijacked' by drug addiction, causing cue-induced cravings and relapse. Similarly, its dysregulation contributes to failed diets, obesity, and eating disorders. Neuroimaging studies in humans have implicated insular cortex in these phenomena. However, it remains unclear how 'cognitive' cortical representations of motivationally relevant cues are biased by subcortical circuits that drive specific motivational states. Here we develop a microprism-based cellular imaging approach to monitor visual cue responses in the insular cortex of behaving mice across hunger states. Insular cortex neurons demonstrate food-cuebiased responses that are abolished during satiety. Unexpectedly, while multiple satiety-related visceral signals converge in insular cortex, chemogenetic activation of hypothalamic 'hunger neurons' (expressing agouti-related peptide (AgRP)) bypasses these signals to restore hunger-like response patterns in insular cortex. Circuit mapping and pathwayspecific manipulations uncover a pathway from AgRP neurons to insular cortex via the paraventricular thalamus and basolateral amygdala. These results reveal a neural basis for state-specific biased processing of motivationally relevant cues.
机译：生理需求偏向感知并关注相关的感觉提示。吸毒成瘾“劫持”了这个过程，导致了线索诱发的渴望和复发。同样，它的失调会导致饮食不当，肥胖和饮食失调。人体的神经影像学研究已将岛状皮层牵涉到这些现象。然而，尚不清楚激励相关线索的“认知”皮质表示如何被驱动特定激励状态的皮质下回路所偏向。在这里，我们开发了一种基于微棱镜的细胞成像方法，以监测行为小鼠在饥饿状态下的岛状皮层中的视觉提示反应。岛状皮层神经元显示出食物引起的反应，在饱腹感时被消除。出乎意料的是，虽然多个饱腹感相关的内脏信号在小岛皮层中会聚，但是下丘脑“饥饿神经元”（表达古迪相关肽（AgRP））的化学生成激活绕过了这些信号，从而恢复了小岛皮层中的饥饿样反应模式。电路作图和通路特异性操作揭示了从AgRP神经元经由脑室旁丘脑和基底外侧杏仁核到岛状皮质的通路。这些结果揭示了动机相关线索的特定于状态的偏向处理的神经基础。

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  • 来源
    《Nature》 |2017年第7660期|611-616|共6页
  • 作者

    Livneh Yoav; Ramesh Rohan N.; Burgess Christian R.; Levandowski Kirsten M.; Madara Joseph C.; Fenselau Henning; Goldey Glenn J.; Diaz Veronica E.; Jikomes Nick; Resch Jon M.; Lowell Bradford B.; Andermann Mark L.;

  • 作者单位

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA|Harvard Med Sch, Program Neurosci, Boston, MA 02115 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA|Harvard Med Sch, Program Neurosci, Boston, MA 02115 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA|Harvard Med Sch, Program Neurosci, Boston, MA 02115 USA;

    Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA|Harvard Med Sch, Program Neurosci, Boston, MA 02115 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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