Neonatal exposure to monosodium glutamate induces cell death and dendritic hypotrophy in rat prefrontocortical pyramidal neurons
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Updated: Oct 10, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
I González-Burgos1, M I Pérez-Vega, C Beas-Zárate
1Laboratorio de Psicobiología, Centro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, A.P. 7-70, C.P. 58261, Morelia, Michoaoán, Mexico. igonbur@hotlaim.com
Abstract:
Monosodium glutamate was administered subcutaneously to male neonate rats, and the effects on cell number and cytoarchitecture of third-layer pyramidal neurons from the prefrontal cerebral cortex were studied in the adult. Monosodium glutamate treatment (4 mg/g of body weight, on post-natal days 1, 3, 5 and 7) resulted in fewer neurons, and shorter and less ramified dendritic processes, than those observed in control animals. Both density and proportional shapes of dendritic spines were not modified. We propose a dual effect of neonatal exposure to glutamate: an excitotoxic effect leading to cell death, and; a secondary neuroprotective effect, arising from the proliferation of glial cells and their subsequent uptake of glutamate, that favors the survival of the remaining neurons, and leads to a further hypotrophic effect on their dendritic processes.

