Reactive astrocytes

Xia M, Qin S, McNamara M, Mackay C, Hyman BT (1997) lnterleukin-8 receptor B immunore-activity in brain and neuritic plaques of Alzheimer s disease. Am J Pathol 150 1267-1274 Xia MQ, Bacskai BJ, Knowles RB, Qin SX, Hyman BT (2000) Expression of the chemokine receptor CXCR3 on neurons and the elevated expression of its ligand IP-10 in reactive astrocytes in vitro ERKl/2 activation and role in Alzheimer s disease. J Neuroimmunol 108 227-235 Xia MQ, Qin SX, Wu LJ, Mackay CR, Hyman BT (1998) Immunohistochemical study of the beta-chemokine receptors CCR3 and CCR5 and their Ugands in normal and Alzheimer s disease brains. Am J Pathol 153 31-37... 

A number of toxic conditions beside hypoosmotic stress and hypoxia/ischemia produce brain edema and the causes may be related to regulation of the aquaporins (see Ch. 34). AQP1 and AQP4 are intensely upregulated in reactive astrocytes in subarachnoid hemorrhage [69], in human glioma and astrocytoma [70] and AQP4 in endothelia and reactive astrocytes in metastatic carcinoma [71,72]. 

Vermeiren C., Najimi M., Vanhoutte N., Tilleux S., de Hemptinne L, Maloteaux J. M., and Hermans E. (2005). Acute up-regulation of glutamate uptake mediated by mGluR5a in reactive astrocytes. J. Neurochem. 94 405 116. 

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, M. Mersel, P. Behr and P. Lutz, Effects of oxysterol treatment on cholesterol biosynthesis and reactive astrocyte proliferation in injured rat brain cortex, J. Neurochem. 65 (1995) 2194-2200. 

Fig. 2. Representative coronal sections of a normothermic and a hypothermic animal 2 mo after 2-h MCAO. Although there is no tissue left in the infarcted area of the normothermic animal, the periinfarct zone still shows reactive astrocytes expressing glial fibrillary acidic protein (GFAP) and manganese-super-oxide dismutase (SOD2) which can be seen as a dark rim around the infarcted area. The hypothermia-treated animal shows a significantly smaller infarct.

Bresjanac M, Antauer G (2000) Reactive astrocytes of the quinolinic acid-lesioned rat striatum express GFRalphal as well as GDNF in vivo. Exp Neurol 764 53-59. 

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