Cholinergic deafferentation after focal cerebral infarct in rats.

Abstract

For a better understanding of neuronal network disturbances after stroke, we investigated the changes in the cholinergic system after experimental focal infarct. We quantitatively evaluated the highly sensitive acetylcholinesterase histochemistry and local glucose utilization 7 days after left middle cerebral artery occlusion in Wistar rats. In all rats with occlusion, the ipsilateral frontal cortex and the nucleus basalis Meynert developed no infarct, whereas the subcortical striatum did. In the frontal cortex on the occlusion side, the acetylcholinesterase-positive fiber density was significantly (p less than 0.05) reduced; a computer-assisted image-analyzing system quantified approximately 1.0 m/mm3 brain cortex acetylcholinesterase-positive fibers in the ipsilateral frontal cortex layers II-IV and approximately 9.7 m/mm3 brain cortex acetylcholinesterase-positive fibers in the contralateral frontal cortex layers II-IV. Local glucose utilization was also significantly (p less than 0.05) decreased in the ipsilateral frontal cortex compared to the contralateral side and sham-operated animals. These results suggest that functional disturbances and disruption of the cholinergic pathway between the frontal cortex and the nucleus basalis Meynert occur after middle cerebral artery occlusion in rats.