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.