Lesions of the entorhinal cortex, which is the major source of afferents to the outer two thirds of the molecular layer of the dentate gyrus, induce an expansion of the commissural projection, which is normally restricted to the inner third, and an intensification of acetylcholinesterase staining in the outer portion of the layer; these changes are thought to be due to the sprouting of the commissural fibers and certain cholinergic afferents to the dentate gyrus, respectively. The authors have studied these sequelae of entorhinal lesions in young adult rats which had been treated with 6-hydroxydopamine (6-OHDA) as neonates, in order to determine whether in the absence of its normal noradrenergic input, morphological plasticity in the dentate gyrus would be altered either in magnitude or extent. In animals treated with 6-OHDA, the levels of noradrenaline in the hippocampal formation were reduced by 93%. Despite this, there was clear evidence for an expansion of the commissural projection following entorhinal lesions, as judged both autoradiographically and in Timm-stained material. Similarly, the intensification of acetylcholinesterase staining in the outer part of the molecular layer appeared as marked as after comparable lesions in untreated animals. From these observations it would appear that in the dentate gyrus, at least, morphological plasticity does not require the presence of an intact noradrenergic innervation.
|Original language||English (US)|
|Number of pages||21|
|Journal||Journal of Comparative Neurology|
|State||Published - 1980|
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