Post-Comprehensive Research Award

• Sharon Idiga (Molecular Medicine Graduate Student, Potthoff lab) - The recent rise in obesity has been greatly influenced by food intake and diet composition. Although multiple studies have explored the complex regulation of macronutrient preference, the molecular mechanisms that govern the appetite for specific macronutrients are largely unknown. Recently, we demonstrated that the pleotropic hepatic endocrine factor, fibroblast growth factor 21 (FGF21), was shown to mediate endocrine control of simple sugar intake and sweet taste preference through its actions in the paraventricular nucleus (PVN) of the hypothalamus. The PVN is comprised of multiple types of neurons, including oxytocin neurons, which project to the ventral tegmental area (VTA), or “reward center” of the brain.  In addition, oxytocin neurons are responsible for the synthesis of oxytocin, and recent evidence revealed that oxytocin plays a role in regulating sweet taste preference. Thus, we hypothesized that FGF21 regulates simple sugar intake and sweet taste preference through its actions on oxytocin neurons in the PVN. Using both gain- and loss-of-function experiments, we show that oxytocin is involved in FGF21 mediating sweet intake and preference. Activation of oxytocin neurons specifically in the PVN using designer receptor exclusively activated by designer drugs (DREADDs) was sufficient to decrease sucrose preference in mice. Conversely, administration of the blood-brain barrier penetrant oxytocin receptor antagonist, L368,899, abrogated the suppression of sugar preference mediated by FGF21. Through these studies, we have identified new mechanistic information into this liver-brain hormonal axis regulating central pathways controlling energy homeostasis and reward.

Ballard Seashore Dissertation Fellowship

• Jacob Rysted (Neuroscience Graduate Student, Usachev lab) - Mitochondria are known as the powerhouse of the cell providing energy for basic biological functions for the body. However, mitochondria are also able regulate calcium signaling inside of cells including neurons where mitochondria calcium regulation has been suggested to play a role in neurotransmission, gene expression, and cell death.  My research investigates how mitochondria calcium regulation contributes to normal neuron function and animal behavior as well as the role of this regulation in neuron pathology such as strokes and seizures.