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1 Biology, Williams College, Williamstown, Massachusetts, United States
* To whom correspondence should be addressed. E-mail: sswoap{at}williams.edu.
Many small mammals have the ability to enter torpor, characterized by a controlled drop in body temperature (Tb). We hypothesized that ghrelin would modulate torpor bouts, as torpor is induced by fasting in mice coincident with elevated circulating ghrelin. Female NIH Swiss mice were implanted with Tb telemeters and housed at an ambient temperature (Ta) of 18 °C. Upon fasting, all mice entered a bout of torpor (minimum Tb: 23.8 ± 2.0 °C). Peripheral ghrelin administration (100 µg) during fasting significantly deepened the bout of torpor (Tb min.: 19.4 ± 0.5 °C). When the arcuate nucleus (ARC) of the hypothalamus, a ghrelin-receptor rich region of the brain, was chemically ablated with monosodium glutamate (MSG), fasted mice failed to enter torpor (min. Tb = 31.6 ± 0.6 °C). Further, ghrelin administration had no effect on the Tb min. of ARC-ablated mice (31.8 ± 0.8 °C). Two major pathways that regulate food intake reside in the ARC, the anorexigenic 
melanocyte stimulating hormone (MSH) pathway and the orexigenic neuropeptide Y (NPY) signaling pathway. Both Ay mice, which have the MSH pathway blocked, and Npy -/- mice exhibited shallow, aborted torpor bouts in response to fasting (Tbmin.: 29.1 ± 0.6 °C and 29.9 ± 1.2 °C, respectively). Ghrelin deepened torpor in Ay mice (Tbmin.: 22.8 ± 1.3 °C), but had no effect in Npy -/- mice (Tbmin.: 29.5 ± 0.8 °C). Collectively, these data suggest that ghrelin’s actions on torpor are mediated via NPY neurons within the ARC.
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