Springer Online Journal Archives 1860-2000
Abstract Previous experiments revealed that the cholinergic deficit in rats with a partial fornix section was accompanied by an increase in turnover of noradrenaline (NE) in the hippocampus. This noradrenergic hyperactivity contributed to the cognitive deficit in lesioned rats, probably by interaction with the cholinergic system. The present experiment examines the reorganization of the noradrenergic system after the damage induced by partial fornix section and attempts to determine if the increase in NE turnover is of locus coeruleus (LC) origin, or if it is a result of local regulation at the noradrenergic terminals. Rats were submitted to knife-cut section of the fornix, resulting in a decrease in choline acetyltransferase activity in the hippocampus, correlated with a significant behavioral deficit in a spatial memory task. Lesioned rats learned a nonspatial memory task normally. Sections of brains of these rats were submitted to quantitative autoradiography. [125I]Iodopindolol binding was assessed in the dorsal and ventral hippocampus to determine availability of β receptors. This was found to be significantly lower in lesioned rats. [125I]Iodoclonidine was used to determine α2 receptors binding in dorsal and ventral hippocampus and in LC. There was no difference in α2 receptors in LC, a significant decrease in dorsal regions of the hippocampus, and a significant increase in ventral regions. Muscarinic M1 receptors in the hippocampus showed no changes after the lesion.
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