Broadly, the Kravitz Lab seeks to understand the neural circuits coordinating complex behaviors, such as those involved in decision making, reward seeking, and ingestion. Recently, we have been studying the circuits that regulate hedonic feeding, which is thought to be a main driver of weight gain in diet-induced obesity. In mice, eating beyond caloric need explains most of the variance in high fat diet (HFD) induced weight gain, rather than differences in metabolic need. To study the circuits that modulate hedonic feeding, our research focuses on the ventral pallidum (VP), a structure linked to motivation and reward expectation.

However, the therapeutic potential to manipulate VP activity to suppress or reverse excessive body weight in obesity remains relatively unexplored. Using the Mightex PolyScan4 GUI and PolyEcho digital acquisition box, we have shown that optogenetic activation of the VP drives voracious feeding for high fat diet, even in sated mice. However, we additionally want to understand the endogenous dynamics of VP neurons during palatable reward consumption. To this end, we used the Mightex OASIS implant to record calcium dynamics from excitatory and inhibitory VP neurons (VPGABA and VPGlu) in awake, head-fixed mice.

We observed proportionally similar levels of activation and inhibition during licking behavior (high calorie Ensure reward) in both VPGABA and VPGlu neurons, however, the activated VPGABA neurons had calcium dynamics that scaled with consumption duration. This suggests that a subpopulation of VPGABA neurons is tuned to palatable reward consumption and might be an ideal mechanistic target for suppressing hedonic feeding that underlies diet-induced obesity.

Mightex Equipment and Software Used:

1. Mightex OASIS Implant (light path and rigid fiber bundle)

2. Mightex BioLED Light Source (BLS-Series 470nm) and liquid light guide

3. Mightex PolyEcho Smart Digital Acquisition Box (DAQ) 4. Mightex PolyScan4 Acquisition GUI