NEUROPEPTIDE CHANGES FOLLOWING EXCITOTOXIC LESION OF THE INSULAR CORTEX IN RATS

Following middle cerebral artery occlusion in Wistar rats, the immunor eactivity of neuropeptide Y increased ipsilaterally in the insular cor tex and basolateral nucleus of the amygdala. In addition, the immunore activity of leucine-enkephalin, dynorphin, and neurotensin increased i n the ipsilateral central nucleus of the amygdala. The amygdalar neuro chemical changes are likely the result of damage to the insular cortex , although other cortical areas were also affected by the ischemia. To investigate whether damage to the insular cortex is essential in elic iting these changes, a localized lesion of the right or left insular c ortex was produced by microinjection of D,L-homocysteic acid. Control animals received injections of vehicle into the right or left insular cortex or D,L-homocysteic acid into the right primary somatosensory co rtex. Neurochemical changes were examined immunohistochemically with t he peroxidase-antiperoxidase reaction 5 days after the injection. The immunoreactivity of neuropeptide Y increased locally after excitotoxic damage to the insular cortex or primary somatosensory cortex. The amy gdalar neurochemical changes, including neuropeptide Y increase in the basolateral nucleus and leucine-enkephalin, dynorphin, and neurotensi n increase in the central nucleus, were seen only when the ipsilateral insular cortex was lesioned. These neurochemical changes were similar to those seen 5 days after middle cerebral artery occlusion. Our find ings indicate that damage to the insular cortex is essential in elicit ing the neurochemical changes in the ipsilateral amygdala. In addition , the change in neuropeptide Y in the cortex appears to be a local rea ction occurring irrespective of location of the lesion and glutamate r eceptor activation may be involved. (C) 1995 Wiley-Liss, Inc.