Volume 82, Number 1, 72-77, DOI: 10.1007/BF00310926

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

K. C. Ma, Z. H. Chang, H. Shih, J. H. Zhu and J. Y. Wu

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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 lsquoreboundrsquo. 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 lsquodeclinersquo illustrate the dynamic plasticity of the reactive astrogliosis.

Key words  Reactive astrogliosis - Portocaval anastomotic encephalopathy - Puncture wound - Compensatory and decompensatory phases of Alzheimer II gliosis

Supported by grant from the National Foundation of Natural Sciences No. 386-0956. This paper was read at the XIth International Congress of Neuropathology, September 7, 1990 in Kyoto, Japan

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