The lateral hypothalamus (LHA) is an important brain region for motivated behaviors including feeding. The LHA contains GABAergic (inhibitory), Glutamatergic (excitatory), and other neuropeptide neuron populations. Previous research demonstrated that optogenetic stimulation of LHA GABA neurons increases food consumption while stimulation of glutamate neurons decreases food consumption, but both populations increase in activity during consumption. The caveats to these previous research experiments are that they do not isolate consummatory behaviors from appetitive behaviors, and they only focus on the role of neuronal stimulation on caloric consumption, not on non-caloric rewards or aversive tastants. In our experiments, we use a multi-spout head-fixed mouse behavioral system to isolate consumption from other behavioral variables, and measure consumption over a range of different concentrations of either rewarding or aversive taste solutions. Using fiber photometry, I recorded calcium dynamics from both neuronal cell types of interest simultaneously, and we found that GABA neuron activity scales with increased lick rate regardless of the solution, while glutamate neuron activity scales with aversive but not rewarding solutions. When I stimulate LHA GABA neurons during consumption using the red-shifted excitatory opsin, Chrimson, we see an increase in licking regardless of solution. Stimulation of LHA vglut2 neurons reduced licking regardless of solution. We also ran inhibition experiments using the red-shifted inhibitory opsin, JAWS, of the two populations and saw that GABA inhibition reduces consumption, while glutamate inhibition increases consumption. Our research has shown how both populations work to drive consummatory behaviors and how their activity level influences consumption. This research is important because it uncovered the function of LHA GABA and Glut neurons in bidirectionally mediating consummatory behaviors for both rewarding and aversive solutions and will contribute to understanding of health issues related to consumption such as obesity.

Human history is marked by intergroup and interpersonal conflict. Over time we have begun to understand that humans, and other animal species, are imperfect decision-makers influenced by learned social biases. Specifically, we are interested in understanding in-group bias: the tendency to favor those of one’s own group over those in other groups. In order to investigate this behavior at the neural circuit and cellular level we developed a social behavior paradigm using male mice. Our paradigm utilizes the resident-intruder assay to determine which social behaviors the resident mouse (C57BL/6J male, n = 16) displays in response to a novel ‘in-group’ (C57BL/6J male) or ‘out-group’ (C57BL/6J albino male) intruder placed in their home cage. We focused on investigative and aggressive behaviors and found that a little over 50% of our resident male mice displayed an out-group aggression bias. This bias was eliminated after early life exposure to a C57BL/6J albino, supporting the hypothesis that this behavior is learned. To better understand the development of in-group bias, our future experiments aim to recapitulate out-group aggression bias without the use of a genetic variant by artificially creating groups with neutral odors. We plan to group-house half of the mice in neutral odor A and the other half in neutral odor B to fabricate an in-group and out-group, and determine whether this model produces out-group aggression bias. These insights will help us to interrogate the neurobiology of aggressive behavior and provide insight on out-group aggression and potential ways to reduce this bias.