Academic Seminars

Linda Rinaman, Ph.D., to present seminar on 4/19/2019 at 11:00 LIB-110: “Gut-Brain Signaling and Motivated Behavior”
April 18, 2019

Linda Rinaman, Ph.D.
Professor of Psychology and Neuroscience
Florida State University

“Gut-Brain Signaling and Motivated Behavior”

Affective anxiety is characterized by behavioral inhibition accompanied by autonomic arousal and vigilance, reflecting a future-oriented emotional state that is generated by perceived threat. Identification of neural circuits that underlie anxiety in animal models is essential for understanding neurobiological mechanisms that contribute to normative and pathological anxiety in humans. Basic and clinical research has emphasized the importance of the central nucleus of the amygdala (CEA) and the anterolateral bed nucleus of stria terminalis (alBST) in regulating the affective and physiological components of anxiety. The CEA and alBST are heavily interconnected via GABAergic and corticotropin releasing-factor (CRF)- expressing neurons, and share many common sources of input, including input from interoceptive (i.e., visceral sensory) brainstem nuclei. Interoceptive feedback from body to brain strongly modulates emotional state, and can elicit anxiety in the absence of environmental threat. Data to be presented will demonstrate the anxiogenic role of a neurochemically discrete interoceptive pathway that targets the CEA-alBST, arising from hindbrain neurons that express glucagon-like peptide-1 (GLP1). GLP1 neurons occupy the most caudal (visceral) portion of the nucleus of the solitary tract (cNST) and medullary reticular formation, where they receive direct and relayed input from vagal and other visceral sensory afferents. GLP1 axon terminals target CEA-alBST subregions that express CRF and GLP1-receptor(R). GLP1 administered centrally or directly into the CEA increases anxiety-like behavior in rats, whereas anxiety is attenuated after central GLP1-R antagonism. GLP1 neurons are robustly activated in rats after ethologically relevant anxiogenic threats that also activate CRF-rich regions of the CEA-alBST, where GLP1 fibers are present. Further, manipulation of interoceptive state by fasting rats overnight blocks the ability of anxiogenic threat to recruit GLP1 neurons, and also significantly attenuates anxiety-like behavior.

Friday, April 19, 2019, 11:00AM-12:00PM, LIB-110
University of North Texas Health Science Center
Fort Worth, Texas