Abstract

A role for glucagon-like peptide-1 (GLP-1) has been postulated in the regulation of blood glucose and satiety. In addition, intracerebroventricular administration of GLP-1 has been shown to suppress locomotor activity, and produce a neuronal activation in the amygdala, a structure involved in mechanisms of fear and anxiety. Adult male Sprague–Dawley rats were prepared with chronic intracerebroventricular cannulae. Measures of experimental anxiety were assessed by the Vogel conflict test and the elevated plus maze. Central GLP-1 (fragment 7–36) administration produces a proconflict effect in the punished drinking test, while leaving measures of activity and nociception unaffected. GLP-1 may participate in the control of fear-induced suppression of behavior, probably via action in the amygdala.

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