Astrocytic and microglia cells reactivity induced by neonatal administration of glutamate in cerebral cortex of the adult rats.
Recent studies confirm that astrocytes and neurons are associated with the synaptic transmission, particularly with the regulation of glutamate (Glu) levels. Therefore, they have the capacity to modulate the Glu released from neurons into the extracellular space. It has also been demonstrated an intense astrocytic and microglia response to physical or chemical lesions of the central nervous system. However, the persistence of the response of the glial cells in adult brain had not been previously reported, after the excitotoxic damage caused by neonatal dosage of monosodium glutamate (MSG) to newborn rats. In this study, 4 mg/g body weight of MSG were administered to newborn rats at 1, 3, 5, and 7 days after birth, at the age of 60 days the astrocytes and the microglia cells were analyzed with immunohistochemical methods in the fronto-parietal cortex. Double labeling to glial fibrillary acidic protein (GFAP) and BrdU, or isolectin-B(4) and BrdU identified astrocytes or microglia cells that proliferated; immunoblotting and immunoreactivity to vimentin served for assess immaturity of astrocytic intermediate filaments. The results show that the neonatal administration of MSG-induced reactivity of astrocytes and microglia cells in the fronto-parietal cortex, which was characterized by hyperplasia; an increased number of astrocytes and microglia cells that proliferated, hypertrophy; increased complexity of the cytoplasm extension of both glial cells and expression of RNAm to vimentin, with the presence of vimentin-positive astrocytes. This glial response to neuroexcitotoxic stimulus of Glu on the immature brain, which persisted to adulthood, suggests that the neurotransmitter Glu could trigger neuro-degenerative illnesses.
Martínez-Contreras
A
A
Lab de Neuroquímica, Div de Neurociencias, C.I.B.O., Guadalajara Jal., Mexico.
Huerta
M
M
Lopez-Perez
S
S
García-Estrada
J
J
Luquín
S
S
Beas Zárate
C
C
D000375:Aging / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D001973:Bromodeoxyuridine; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002540:Cerebral Cortex / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D005455:Fluorescent Antibody Technique; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D037102:Lectins; D008297:Male; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D009498:Neurotoxins / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013234:Stem Cells / Q000187:drug effects / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology; D014746:Vimentin / Q000378:metabolism
D005904:Glial Fibrillary Acidic Protein; D037102:Lectins; D009498:Neurotoxins; D014746:Vimentin; D018698:Glutamic Acid; D001973:Bromodeoxyuridine