COLCHICINE AFFECTS CORTICAL AND AMYGDALAR NEUROCHEMICAL CHANGES DIFFERENTIALLY AFTER MIDDLE CEREBRAL-ARTERY OCCLUSION IN RATS

Recently, we have shown increases in the immunoreactivity for neuropep tide Y and tyrosine hydroxylase in the insular cortex surrounding the focal infarction after middle cerebral artery occlusion. In addition, the immunoreactivity for neuropeptide Y, leucine-enkephalin, dynorphin , and neurotensin increased ipsilaterally in the amygdala. Increases i n immunoreactivity were observed in nerve terminals and fibers; change s in the neuropeptides were maximal 3 days after stroke. Local excitot oxic injury of the insular cortex also elicited similar neuropeptide c hanges unilaterally in the same regions. In this study, immunohistoche mistry was used following intracerebroventricular injection of colchic ine and stroke to determine whether blockade of axonal transport would prevent these neurochemical changes. These experiments would also loc ate the putative cellular origins of the neurochemicals involved. Cont rol rats received either colchicine injection or middle cerebral arter y occlusion alone. Injection of colchicine enhanced the periinfarct in crease in neuropeptide Y but did not alter the increase in tyrosine hy droxylase. The neuropeptide Y increase was observed in local cortical neurons. Colchicine prevented the increases in immunoreactivity for th e neuropeptides in the amygdala on the side of stroke, although there were small perikarya that showed immunoreactivity for these neuropepti des within the amygdala on both sides. We conclude that local cortical neurons are responsible for the increase in neuropeptide Y in the per iinfarct region, that the cortical increase in tyrosine hydroxylase is not dependent on fast axonal transport, and that axonal transport of signals from the insular cortex to the amygdala is critical in mediati ng the amygdalar neuropeptide changes seen after stroke. (C) 1997 Wile y-Liss, Inc.