The role of medial basal glutamatergic neurons to control metabolism during exercise and recovery.

We have observed dynamic medial basal hypothalamic activation after exercise in POMC and NPY/AgRP neurons, and we have observed changes in metabolism during manipulation of medial basal glutamatergic neurons, particularly under the energy deficit condition caused by fasting. However, it is unclear if energy deficit from exercise could also have a similar effect. This proposal 1) seeks to test if exercise induced energy expenditure/recovery activates medial basal glutamatergic neurons and 2) if medial basal hypothalamic glutamatergic neuron manipulation contribute to food intake in an energy deficit dependent fashion. Based on our preliminary data, we expect that activation of medial basal glutamatergic neuron will induce feeding behavior to compensate for energy deficit by increased food intake, but will have no effect in sedentary mice. The physiological role of this neuron population will be reflected by increased neuronal depolarization marker during exercise recovery, associated with our preliminary data of exercise induced NPY activation.

Scholars @ ECU