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Effects of Leptin on the Firing Rates of Thermoregulatory Neurons in the Anterior Hypothalamus
Author(s) -
Hack Laura M,
Griffin John D
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1247-a
Subject(s) - leptin , hypothalamus , medicine , endocrinology , appetite , hormone , set point , leptin receptor , energy expenditure , hyperthermia , chemistry , biology , obesity , control engineering , engineering
The hormone leptin is postulated to play a major role in body fat regulation in many mammalian species (Cohen, 2001). Leptin is produced by adipocytes and circulates throughout the bloodstream in an amount proportional to total body fat percentage. When leptin binds to its receptors on hypothalamic neurons, it leads to a decrease in food intake and an increase in energy expenditure (Ahima, 2000). Luheshi et al. (1999) reported that when leptin was injected into rats in an amount high enough to suppress appetite, it also produced hyperthermia. This leptin dependent change in temperature may be one mechanism whereby leptin suppresses appetite. Our project attempted to determine the mechanism by which leptin increases body temperature. We hypothesized that leptin would increase the firing rates of temperature insensitive neurons and decrease the firing rates of warm sensitive neurons in the anterior hypothalamus. Based on current models of thermoregulatory control, these responses would lead to hyperthermia (Boulant, 1980). Using a hypothalamic tissue slice preparation, single‐unit recordings allowed neurons to be thermally classified. Tissue slices were then perfused with the active portion of the leptin hormone (100 nM). Our data analysis indicates that warm sensitive neurons decrease their firing rates in response to leptin, whereas the majority of temperature insensitive neurons increase their firing rates. These findings are consistent with a hyperthermic shift in set point temperature. (Supported by NSF: IBN‐9983624, and in part by a Howard Hughes Medical Institute grant through the Undergraduate Biological Sciences Program to the College of William and Mary)