Glial fibrillary acidic protein messenger RNA and glutamine synthetase activity after nervous system injury

Abstract

The level of the mRNA for glial fibrillary acidic protein (GFAP), the major protein of the intermediate filaments of astroglial cells, and the activity of glutamine synthetase (GS), an enzyme selectively localized in astrocytes, were measured at different times after a unilateral mechanical lesion in the rat cerebral cortex. A rapid and early increase (6 hours post-lesion) in GFAP mRNA was observed; GFAP mRNA level reached a peak at 1-3 days and then decreased. Moreover, an astrocytic activation in cortical zones far from the injury site and in the contralateral hemisphere was detected. No change of GS activity was observed in the same model of brain injury, showing that this astroglial marker is not modified during the reactive gliosis obtained with this experimental model. GFAP mRNA has also been detected in the rat sciatic nerve; however, its level was not modified after nerve transection, suggesting a different regulation of GFAP expression in the peripheral nervous system.

Proinflammatory cytokine synthesis in the injured mouse spinal cord: Multiphasic expression pattern and identification of the cell types involved

“…One possible consequence of the rapid and widespread expression of IL-1␤ and TNF could be the modulation of astrogliosis. It is noteworthy that astrocytes located around the lesion site and in areas distal from the traumatic injury rapidly produce increasing amounts of the intermediate filament GFAP mRNA (within 6 hours) and protein (within 12 hours) (Condorelli et al, 1990;Yong, 1996), undergo hypertrophy, and extend their processes. Also of relevance in light of our results are earlier studies reporting that the initial astrocytic reaction may extend up to 10 mm from the site of SCI in rats (Eng et al, 1987;Reier and Houle, 1988).…”

Expression of neuronal markers, synaptic proteins, and glutamine synthetase in the control and regenerating lizard visual system

“…In regeneration-deficient systems such as the mammalian CNS, GS activity increases in the injured ON (Politis and Miller, 1985) and spinal cord (Benton et al, 2000). Conversely, its expression is downregulated in the detached retina (Lewis et al, 1994) and remains unchanged in the injured cerebral cortex (Condorelli et al, 1990). In regeneration-competent systems such as the rat peripheral nerve, GS activity decreases after axotomy (Politis and Miller, 1985).…”

Oxystdrol (7β‐hydroxycholestesteryl‐3‐oleate) promotes serotonergic reinnervation in the lesioned rat spinal cord by reducing glial reaction

“…This increase occurs at the site of injury as well as in regions distant to the initial site of the lesion (Bignami and Dahl, 1976;Takamiya et al, 1988;Tetzlaff et al, 1988). However, the expression of mRNA for GFAP follows a different time course during normal development and after injury (Tardy et al, 1989;Condorelli et al, 1990;Hozumi et al, 1990;Steward et al, 1990). A rapid increase in GFAP mRNA precedes a significant increase in GFAP, and the decrease of message is more precipitate than the slow decline of GFAP content (Hozumi et al, 1990;Steward et al, 1993).…”

“…It appears that the relative importance of these two components of the astrocytic reaction is dependent on specific injuries, particular regions of the CNS, and on the state of maturation (Hatten et al, 1991). These changes are correlated with an increase in GFAP-IR and GFAP mRNA expression (Bignami and Dahl, 1976;Privat et al, 1981;Takamiya et al, 1988;Condorelli et al, 1990;Steward et al, 1990Steward et al, , 1993Kost-Mikucki and Oblinger, 1991;Cancilla et al, 1992;Landry et al , 1992). The result of this astrocytic reaction is the formation of a dense astrocytic scar which is usually considered to be a physical barrier to axonal regeneration (Carlstedt, 1985;Reier et al, 1983;Stensaas et al, 1987).…”