Astrocytic and microglia cells reactivity induced by neonatal administration of glutamate in cerebral cortex of the adult rats

Abstract

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.

Critical Role for Akt1 in the Modulation of Apoptotic Phosphatidylserine Exposure and Microglial Activation

“…Proliferating cell nuclear antigen (PCNA) staining for microglial activation (Williams et al, 2002) and bromodeoxyuridine (BrdU) staining for microglial proliferation (Martinez-Contreras et al, 2002) was performed with anti-mouse monoclonal antibody PCNA (1:100) or BrdU (1:100) conjugated with biotinylated anti-mouse IgG (1:50) and visualized through fluorescein avidin (1:50) for PCNA and Texas Red streptavidin (Vector Laboratories) for BrdU. BrdU (10 M) and fluorodeoxyuridine (1 M; Sigma, St. Louis, MO) were applied 1 h before the time of fixation.…”

Cellular demise and inflammatory microglial activation during β-amyloid toxicity are governed by Wnt1 and canonical signaling pathways

“…In Fig. 3B, representative microglial cultures illustrate a marked induction of microglial activation and proliferation during treatment with Aβ 1-42 exposed media from SH-SY5Y wildtype cells (Aβ ) as evidenced by significant PCNA expression [24] and BrdU uptake [25] when compared to microglia treated with media not exposed to Aβ 1-42 (Control). Minimal activation (PCNA) or proliferation (BRDU) of microglia is present during treatment with media from SH-SY5Y cells overexpressing Wnt1 (Wnt1/Aβ ) which are also absent of membrane PS exposure (Fig.…”

Influence of the age of rats treated with the sodium salt of glutamate acid on the reactivity of astroglia of the infundibular nucleus

“…W licznych badaniach wykazano, że systematyczne podawanie soli sodowej kwasu glutaminowego neonatalnym szczurom prowadzi do uszkodzenia struktur nerwowych wielu obszarów OUN (2,6,20,25). Młode zwierzęta są bardziej wrażliwe na toksyczne działanie Glu w porównaniu do osobników dorosłych, co należy wiązać ze stopniem rozwoju i przepuszczalności bariery krew-mózg (blood-brain barrier -BBB).…”

“…Dodatkowo inni autorzy zaobserwowali, że podskórne podanie MSG nowo narodzonym szczurom indukuje podział astrogleju np. w korze czołowo--ciemieniowej (20). Astrocyty najintensywniej dzielą się ok. 3.-4. dnia po zadziałaniu czynnika uszkadzającego, co obserwowano w przebiegu wielu procesów patologicznych OUN.…”