The perforant path (entorhino-dentate fibers) which terminates in the outer parts of the molecular layer of fascia dentata, was transected in adult rats. After 2–93 days survival, serial cryostat sections were prepared and either stained for acetylcholinesterase (AChE), cell bodies (thionin) and degenerating nerve terminals (Fink-Heimer), or freeze-dried for biochemical assay of choline acetyltransferase (ChAc), AChE and glutamate decar☐ylase (GAD). There was a 50–60% increase in the activities of ChAc and AChE per weight or volume of tissue in the molecular layer of fascia dentata, being specifically localized to the zones where the degenerating nerve terminals are found. The increase was already fully developed at 8 days survival. Simultaneously, there was a moderate increase in GAD per amount of tissue, significantly smaller than that of ChAc and AChE. The latter effect was probably caused by the shrinkage of tissue due to loss of perforant path elements. Concomitantly with these changes there was an increase in width of the AChE-poor zone in the inner part of the molecular layer, which normally contains the terminals of the commissural and ipsilateral afferents from hippocampus (CA3). Transection of the septal afferents showed that the nerve elements responsible for the increased ChAc and AChE activities were of the same origin as the cholinergic elements normally present. Transection of another important afferent route to the fascia dentata, the commissural fibers, led to no changes in AChE staining. The results indicate that in response to degeneration of the afferents from the entorhinal area there occurs a reorganization of the nerve elements in the molecular layer of fascia dentata, including a relative increase of the cholinergic nerve terminals and axons.
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