We have found that estrogen promotes suppression of feeding and a lean body mass while activating the arcuate nucleus proopiomelanocortin (POMC)-expressing neurons. These neurons, when activated, suppress appetite and increase energy expenditure. Because the increased activation of POMC neurons by estradiol was associated with increased glutamate receptor presence that enable calcium influx, we analyzed the expression of the calcium-binding protein, parvalbumin, in these hypothalamic neurons. We observed that estrogen treatment of female mice resulted in induction of parvalbumin-immunoreactivity in arcuate nucleus neurons, a large number of which was POMC-expressing. These data indicate that the increased excitatory activity induced by estradiol in the arcuate nucleus in support of suppression of appetite is associated with calcium overload of these neurons. Although parvalbumin may protect these cells from calcium overload-associated neuronal degeneration, maintenance of calcium entry may lead to increased vulnerability of POMC neurons during the course of sustained satiety.
ASJC Scopus subject areas
- Obstetrics and Gynaecology