TRAUMATIC LESIONS AND TRANSPLANTS OF GRANULE CELLS IN THE DENTATE GYRUS ALTER THE DISTRIBUTION OF AFFERENT-FIBERS IN THE MOLECULAR LAYER

The present experiments determined whether traumatic lesions of the de ntate gyrus granule cells had a different effect on the afferents in t he molecular layer (ML) than nontraumatic lesions. Nontraumatic lesion s of the granule cells induced by colchicine, ibotenic acid, x-radiati on, and adrenalectomy have been reported to reduce both the acetylchol inesterase (AChE)-positive fibers and entorhinal afferents in the ML. After the nontraumatic granule cell lesions, the laminar distribution of the entorhinal afferents was maintained in the ML, whereas the AChE laminar pattern was lost. In the present study, dentate granule cells were traumatically lesioned by a fluid injection into the infragranul ar cleavage plane (IGCP) of the dentate gyrus. The traumatic lesion re sulted in an altered distribution of the afferents in the MIL. The per forant path fibers, shown by injection of wheat germ agglutinin horser adish peroxidase into the entorhinal cortex, occupied a greater propor tion of the ML in lesioned animals than in control animals. The normal laminar pattern of AChE-positive afferents was not present after the granule cell lesion. There was an initial increase in AChE-positive fi bers in the ML that lasted several weeks but eventually returned to ne ar normal levels. The altered distribution of afferents could in part be due to uneven shrinkage of the molecular layer and/or sprouting of the afferents. Granule cell suspension transplants into the IGCP also traumatically lesioned the host granule cells but immediately replaced the damaged host granule cells with immature granule cells. The distr ibution of afferents was similar to that found in lesioned-only animal s. The traumatic lesion induced MAP2 immunoreactivity in the anisomorp hic reactive astrocytes of the ML. At the longer survival times, MAP2 was not seen in either the astrocytes of the ML or in the isomorphic r eactive astrocytes in CA3.