Genetically Dissecting Basal Forebrain Circuits Underlying Eating Disorders
Abstract
Abnormal eating habits that drive excessive food seeking- or avoidance can manifest as health-threatening and socially impactful eating disorders. The scope of research includes 3 main aims: 1) to determine how basal forebrain ACh+ and Glu+ neurons are connected; 2) to determine how Glu+ neurons in the basal forebrain influence feeding behavior; and 3) to identify downstream targets of basal forebrain Glu+ neurons that govern feeding behavior. Specific results from this reporting period have identified that specific activation of DBB Glu+ neurons severely reduced feeding, and importantly, specific activation of DBB Glu+ fibers in the lateral hypothalamus (LH) also induced similar reduction in feeding, suggesting LH as one major downstream target mediating the feeding effect. However, specific inhibition of DBB Glu+ fibers in LH failed to increase feeding, suggesting a sufficient but not necessary role for LH neurons in mediating the feeding effect. The remaining planned experiments including the examination of local DBB circuits between cholinergic and glutamatergic neurons, the genetic interaction between DBB Glu+ neurons and the ob gene and the effect of DBB Glu+ neurons in motivation feeding will be accomplished in the next year. Overall, the results of the supported work will provide insights on how basal forebrain ACh+ and Glu+ neurons are connected, how Glu+ neurons in the basal forebrain influence feeding behavior and related behaviors and identify the downstream targets that mediate basal forebrain Glu+ neurons in regulating eating and related behaviors.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2022
- Accession Number
- AD1196917
Entities
People
- Tong Qingchun
Organizations
- University of Texas Health Science Center at San Antonio