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.