Evidence for bidirectional dendritic transport of horseradish peroxidase.
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Biomedical subjects
Publications and source records attributed to G Lynch.
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Lesions of the entorhinal cortex in neonatal rats cause the commissural projections to the dentate gyrus to spread from their normal location in the inner molecular layer into the outer molecular layer, a region normally occupied by afferents from the entorhinal cortex. These lesions also cause the short-latency response to commissural stimulation to spread into the outer molecular layer, a result suggesting that these abnormally located connections are operative.
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In immature animals, ablation of the entorhinal cortex elicited a rapid intensification of acetylcholinesterase (EC 3.1.1.7) staining in the outer one-quarter of the molecular layer of the dentate gyrus. Subsequent lesions of the septum eliminated this acetylcholinesterase intensification. Electron-microscopic histochemical analysis demonstrated a 30-fold increase in the number of acetylcholinesterase-positive synaptic endings in the intensification zone. The acetylcholinesterase augmentation thus appears attributable, in part at least, to an increase in the number of acetylcholinesterase-rich synaptic endings established by septo-hippocampal fibers. Observations in a comparative study of immature and adult rats point to the animal's developmental state as a major determinant of differences in these lesion-induced neuronal adjustments.
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