Glial changes in the progress of a chemical lesion. An electron microscopic study.
The response of non-neuronal cells in the brain to monosodium glutamate (MSG) was studied in the neonatal mouse brain. Neurons rapidly degenerate in this chemically-induced lesion, and the glia reflect and respond to their early pyknosis and death. Astrocytic glia exhibit the most profound responses in the form of degenerative nuclear and cytoplasmic changes within 15 to 20 minutes after ingestion of MSG. After 6 to 12 hours, a large glial cell population, containing neuronal and synaptic debris, can be seen. Recovery of severely damaged astrocytes is unlikely. Further, evidence of multiplication of uninjured cells to supply this observed repopulation was found. Microglia start to engulf debris at 6 to 12 hours and continue this process through at least 48 hours. From 3 to 48 hours, a third cell type, tentatively identified as a Gitter cell, is preminently involved in phagocytosis of neuronal elements. Nuclei of these cells enlarge and their parikarya become vastly expanded in a fashion typical of Gitter cells. These cells appear to represent the transformed microglia. Phagocytosis following a chemical lesion induced by glutamic acid, a neurotransmitter substance, is exceedingly rapid in comparison to that elicited by other types of lesions. Further, endogenous glial cells cope with the cellular debris; no participation in this process by hematogenous cells was observed.
D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000648:ultrastructure; D001927:Brain Diseases / Q000139:chemically induced / Q000473:pathology; D051379:Mice; D009457:Neuroglia / Q000648:ultrastructure*; D012970:Sodium Glutamate; D013569:Synapses / Q000648:ultrastructure; D013787:Thalamic Nuclei / Q000473:pathology*
D012970:Sodium Glutamate