RT Journal Article SR Electronic T1 CNS Glucagon-Like Peptide-1 Receptors Mediate Endocrine and Anxiety Responses to Interoceptive and Psychogenic Stressors JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 6163 OP 6170 DO 10.1523/JNEUROSCI.23-15-06163.2003 VO 23 IS 15 A1 Kinzig, Kimberly P. A1 D'Alessio, David A. A1 Herman, James P. A1 Sakai, Randall R. A1 Vahl, Torsten P. A1 Figueiredo, Helmer F. A1 Murphy, Erin K. A1 Seeley, Randy J. YR 2003 UL http://www.jneurosci.org/content/23/15/6163.abstract AB Responses to stressors serve to adjust physiology and behavior to increase short-term survival at the potential expense of increasing susceptibility to disease over the long term. We show that glucagon-like peptide-1 (7–36) amide (GLP-1) increases levels of the stress-activated hormones ACTH and corticosterone when administered directly into the rat brain and increases levels of anxiety as measured by the elevated plus maze. The endocrine response is preferentially activated by GLP-1 administration in the paraventricular nucleus of the hypothalamus, whereas the anxiety response is preferentially activated by administration in the central nucleus of the amygdala. Furthermore, GLP-1 antagonists block increases in stress hormones associated with the toxin LiCl and both the endocrine and anxiety responses to vertical heights. Although diverse neural circuits must necessarily process disparate stressors, the current data implicate a role for the GLP-1 system as a critical mediator of multiple stress responses.