The compensatory ?rebound? of reactive astrogliosis: glial fibrillary acidic protein immunohistochemical analysis of reactive astrogliosis after a puncture wound to the brain of rats with portocaval anastomosis

Abstract

This study was designed to compare the degree of reactive astrogliosis occurring around a puncture wound in the brain of normal rats and at different intervals after a similar puncture wound in rats with a portocaval anastomosis. The gliosis was evaluated by the number of astrocytes, the thickness of their processes and the intensity of the glial fibrillary acidic protein immunoreactivity. After the puncture wound in the brain of rats with a portocaval anastomosis, the gliosis varied at different intervals being: (1) decreased at 10 days, (2) markedly increased at 5 weeks and (3) significantly decreased at 8, 12, and 16 weeks. These findings suggest that 5 weeks after portocaval anastomosis, an active proliferation of the metabolically altered astrocytes occurs with heightened synthesis of glial fibrillary acidic protein in the period of adaptive compensation, the so-called compensatory 'rebound'. At 8 weeks or more after portocaval anastomosis, these altered astrocytes were considered to be in the phase of decompensation and incapable of maintaining the reactive response which occurred in normal rats. The compensatory rebound and decompensatory 'decline' illustrate the dynamic plasticity of the reactive astrogliosis.

Safety of Direct Administration of AAV2CUhCLN2, a Candidate Treatment for the Central Nervous System Manifestations of Late Infantile Neuronal Ceroid Lipofuscinosis, to the Brain of Rats and Nonhuman Primates

“…This suggests that all of the abnormal histopathology that arises is a result of the needle insertion and that the infusion rate and test object cause no additional histopathology. This is corroborated in multiple studies in which extensive gliosis has been observed at the site of needle insertion into the brain (Ma et al, 1991;Lo et al, 1999;Xue and Del Bigio, 2001). In addition, there is rapid infiltration of macrophages after needle trauma that may not be seen in this study because by 1 week microglial cells are more prevalent (Kaur et al, 1987;Fujita et al, 1998).…”

Rats with minimal hepatic encephalopathy due to portacaval shunt show differential increase of translocator protein (18 kDa) binding in different brain areas, which is not affected by chronic MAP-kinase p38 inhibition

“…There is a good number of studies on the effects of PCS on astrocytes, showing changes that are different in depending on the brain region (Bodega et al 1991; Suárez et al 1997) and on the time after PCS surgery (Ma et al 1991). In general these studies show enlarged nuclear size (Diemer and Laursen 1977), increased astrocyte cell and cytoplasmic area (Laursen and Diemer 1980) and no evidence of Alzheimer type II cells (Pilbeam et al 1983).…”

Construction and Implantation of a Microinfusion System for Sustained Delivery of Neuroactive Agents.

“…Adjacent 70 µm sections underwent a standard immunofluorescence procedure to detect glial fibrillary acidic protein (GFAP), which is expressed by astrocytes during the process of reactive gliosis in response to trauma (Ding et al, 2000;Ma et al, 1991). Briefly, free-floating sections were rinsed with PBS and blocked with 10% normal donkey serum (NDS) and 3% bovine serum albumin in 0.1 M PBS with 0.3% Triton X-100 (PBS/Triton) for one hour and then incubated in rabbit anti-GFAP antibody (1:500; Sigma Chemical Co., St. Louis, MO) in PBS/Triton with 1% NDS for 12 hours at 4°C.…”