Post: USC’s DORI Seminar (Friday, January 27, 2023): Sung-Yon Kim, PhD

Happy New Year’s! Please join us for USC’s DORI Seminar on Friday, January 27, 2023 at 12 pm in-person at UPC.

Warm and Full: Neural Circuits for Behavioral Regulation of Homeostasis

Many of our behaviors are intrinsically motivated by a need to maintain homeostasis, including that of body temperature, energy, and fluid levels. Despite their importance, numerous seemingly simple questions remain unresolved in this field. My presentation will focus on our ongoing efforts to address two of these issues in mouse models.

The first part attempts to address: How do we turn on the heat when it is cold? Thermoregulatory behavior is among the least-studied classic motivated behaviors—until recently, no forebrain region or cell type was shown to be necessary for these responses. We recently identified the lateral hypothalamus (LH) and its Vgat+ neurons as a necessary region and cell type (Jung et al., Neuron 2022). LH Vgat+ neurons encode thermoregulatory behavior, as well as the reward value of thermal stimuli, and parabrachial inputs are required for both this encoding and thermoregulatory behavior. Notably, two-photon Ca2+ imaging revealed distinct LH Vgat+ subpopulations encoding thermal and caloric rewards. The functional heterogeneity within the LH Vgat+ population will be discussed in detail.

The second part tries to answer: How do we stop eating when we are “mechanically” full? Mechanosensory feedback from the digestive tract to the brain is critical for limiting excessive food and water intake, but the underlying gut-brain communication pathways and mechanisms remain poorly understood. We found that Pdyn+ neurons in the parabrachial nucleus monitor the intake of both fluids and solids, using mechanosensory signals arising from the upper digestive tract (Kim et al., Nature 2020; also see Kim et al., Nat Rev Neurosci 2022). Upon receipt of the mechanosensory signals, these neurons produce aversive and sustained appetite-suppressing signals that serve as negative feedback on ingestion to prevent harmful overconsumption. Our continuing efforts to pinpoint the precise site of the origin of mechanosensory feedback signals and the downstream circuit that integrates these signals with appetite-promoting signals will also be described.

In sum, our findings lay the groundwork for future research into the neural bases of behavioral thermoregulation and mechanosensory feedback control of ingestion, as well as their relationships with other motivated behaviors.

Please join us live at UPC:

Hedco Neuroscience Building

3641 Watt Way, HNB 107

Los Angeles, Ca 90089-2520

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