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Food intake behavior is regulated by a network of appetite-inducing and appetite-suppressing neuronal populations throughout the brain. The parasubthalamic nucleus (PSTN), a relatively unexplored population of neurons in the posterior hypothalamus, has been hypothesized to regulate appetite due to its connectivity with other anorexigenic neuronal populations and because these neurons express Fos, a marker of neuronal activation, following a meal. However, the individual cell types that make up the PSTN are not well characterized, nor are their functional roles in food intake behavior. Here, we identify and distinguish between two discrete PSTN subpopulations, those that express tachykinin-1 (PSTN Tac1 neurons) and those that express corticotropin-releasing hormone (PSTN CRH neurons), and use a panel of genetically encoded tools in mice to show that PSTN Tac1 neurons play an important role in appetite suppression. Both subpopulations increase activity following a meal and in response to administration of the anorexigenic hormones amylin, cholecystokinin (CCK), and peptide YY (PYY). Interestingly, chemogenetic inhibition of PSTN Tac1 , but not PSTN CRH neurons, reduces the appetite-suppressing effects of these hormones. Consistently, optogenetic and chemogenetic stimulation of PSTN Tac1 neurons, but not PSTN CRH neurons, reduces food intake in hungry mice. PSTN Tac1 and PSTN CRH neurons project to distinct downstream brain regions, and stimulation of PSTN Tac1 projections to individual anorexigenic populations reduces food consumption. Taken together, these results reveal the functional properties and projection patterns of distinct PSTN cell types and demonstrate an anorexigenic role for PSTN Tac1 neurons in the hormonal and central regulation of appetite.more » « less
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Berman, Justin D; Randeria, Manjari; Style, Robert W; Xu, Qin; Nichols, James R; Duncan, Aidan J; Loewenberg, Michael; Dufresne, Eric R; Jensen, Katharine E (, Soft Matter)We characterize the mechanical recovery of compliant silicone gels following adhesive contact failure. We establish broad, stable adhesive contacts between rigid microspheres and soft gels, then stretch the gels to large deformations by pulling quasi-statically on the contact. Eventually, the adhesive contact begins to fail, and ultimately slides to a final contact point on the bottom of the sphere. Immediately after detachment, the gel recoils quickly with a self-similar surface profile that evolves as a power law in time, suggesting that the adhesive detachment point is singular. The singular dynamics we observe are consistent with a relaxation process driven by surface stress and slowed by viscous flow through the porous, elastic network of the gel. Our results emphasize the importance of accounting for both the liquid and solid phases of gels in understanding their mechanicsmore » « less
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