Abstract
Hypothalamic tanycytes are chemosensitive glial cells that contact the cerebrospinal fluid in the third ventricle and send processes into the hypothalamic parenchyma. To test whether they can activate neurons of the arcuate nucleus, we targeted expression of a Ca2+-permeable channelrhodopsin (CatCh) specifically to tanycytes. Activation of tanycytes ex vivo depolarized orexigenic (neuropeptide Y/agouti-related protein; NPY/AgRP) and anorexigenic (proopiomelanocortin; POMC) neurons via an ATP-dependent mechanism. In vivo, activation of tanycytes triggered acute hyperphagia only in the fed state during the inactive phase of the light-dark cycle.
Highlights
(proopiomelanocortin; POMC) neurons via an ATP-dependent mechanism
To test the effect of activating just a single tanycyte, we loaded tanycytes with Rhod-2 AM and exploited the fact that a brief exposure to infrared illumination (720 to 730 nm) within a region of interest (ROI) smaller than the soma can evoke a localized elevation of intracellular Ca2+ in that ROI (Fig. 1, SI Appendix, Fig. S1, and Movies S1–S3)
We demonstrate that tanycytes, engineered to express channelrhodopsin, can activate arcuate neurons to induce acute hyperphagia when activated by light
Summary
(proopiomelanocortin; POMC) neurons via an ATP-dependent mechanism. In vivo, activation of tanycytes triggered acute hyperphagia only in the fed state during the inactive phase of the light–dark cycle. There has been particular interest in hypothalamic tanycytes, a specialized type of glial cell, that line the third ventricle Their cell bodies contact the cerebrospinal fluid (CSF) and send a single process into the hypothalamic parenchyma reaching nuclei such as the ARC and the ventromedial hypothalamic nuclei [12, 13]. Direct evidence for these cells communicating with the central primary effectors of feeding (arcuate AgRP/NPY and POMC neurons) to influence food intake is lacking. We have addressed this question by targeting expression of a Ca2+-permeable version of channelrhodopsin (CatCh) via a cell-specific promoter to tanycytes to permit their specific activation by light. To further understand the role of tanycytes in the hypothalamic neuronal network controlling food intake, we studied the effect of tanycyte activation during the inactive (light) phase of the light–dark cycle and following a 19-h period of fasting
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