Reactive gliosis

It is well accepted that MDMA produces 5-HT depletions in rat CNS, but much less attention has been devoted to the effects of MDMA on established markers of neurotoxicity such as cell death, silver-positive staining, and reactive gliosis. Support for the hypothesis of MDMA-induced axotomy relies heavily on immunohistochemical analysis of 5-HT levels, which could produce misleading results if not validated by other methods. For example, MDMA-induced loss of 5-HT could be due to persistent adaptive changes in gene expression or protein function, reflecting a state of metabolic quiescence rather than neurotoxic damage. Table 7.3 summarizes the effects of MDMA on hallmark measures of neurotoxicity. 

As another application of LCM to CNS injury, Ho et al. (ref. 533) studied the affinity of LCM to the site of a localized (thermal) brain injury. It had been well documented that in response to injury in the CNS, astrocytes are activated which is accompanied by an increased content of GFAP, hypertrophy, and hyperplasia (ref. 679-683). (This process of gliosis (ref. 682) results in scar formation it has been speculated that the scar may inhibit axonal regeneration (ref. 684)) (ref. 533). Ho et al. observed that the influx of LCM began at the time when GFAP-positive cells began to appear. It seemed likely that LCM are initially attracted to the reactive astrocytes, but subsequently the LCM were found to be excluded... 

D. Bochelen, F. Eclancher, A. Kupferberg, A. Privat and M. Mersel, 7(5-hydroxycholesterol and 7p-hydroxycholesteryl-3-esters reduce the extent of reactive gliosis caused by an electrolytic lesion in rat brain, Neuroscience 51 (1992) 827-834. 

Astrocyte activation or reactive gliosis involves proliferation, recruitment to the site of injury (Walton et al, 1999), and release of numerous cytotoxic agents including proteolytic enzymes, cytokines, complement proteins, reactive oxygen intermediates, NMDA-like toxins, and nitric oxide (Weldon et al, 1998). Sarin exposure activated astrocytes... 

Martins, R.N., Taddei, K., Kendall, C., Evin, G., Bates, K.A., Harvey, A.R. (2001). Altered expression of apolipoprotein E, amyloid precursor protein and presenilin-1 is associated with chronic reactive gliosis in rat cortical tissue. Neuroscience 106 557-69. 

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