Astrocytes activation

V. Mechanism of M3G-Induced Allodynia Spinal Astrocyte Activation... 

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... 

Figure 8.4. Expression of iNOS by various pro-inflammatory cytokines in human primary astrocytes. TNF- bdotalpha and IFN-y alone or in combination are unable to induce the expression of iNOS. On the other hand, IL-IB alone or in combination with other cytokines induce iNOS in human astrocytes. Activation of AP-1 and GAS together by IFN-y is not sufficient for the expression of iNOS. Activation of AP-1 and NF-kB together by TNF-a is also not sufficient for iNOS expression. Activation of AP-1, NF-kB and GAS together even at a higher level by the combination of TNF-a and IFN-y compared to that induced by individual cytokines is also not sufficient for the expression of iNOS. However, 11-1(3 capable of activating C/EBP(3, AP-1 and NF-kB induced iNOS in human astrocytes suggesting an important role of C/EBP(3 in the expression of iNOS in human astrocytes.

Tani M, Glabinski AR, Tuohy VK, Staler MH, Estes ML, Ransohoff RM (1996) In situ hybridization analysis of ghal fibrillary acidic protein mRNA reveals evidence of biphasic astrocyte activation during acute experimental autoimmune encephalomyelitis. Am J Pathol 148 889-896. 

Hall ED, Oostveen JA, Gurney ME (1998) Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALS. Glia 23 249-256. 

The nasal administration of Aft in PDAPP mice has also been described (120). Weekly administration of A/S40 (25 /ig), beginning at age 5 months and continuing until age 12 months, was associated with a 60% reduction in plaque burden in the hippocampus, decreased neuritic dystrophy, and a reduced level of microglial and astrocytic activation. The presence of anti-A/3 antibodies was demonstrated in the serum of immunized mice, and a slight mononuclear cell infiltration in brain tissue was characterized by cytokine expression. 

Pekny, M., Wilhelmsson, U., Pekna, M., 2014. The dual role of astrocyte activation and reactive gliosis. Neurosci. Lett. 565, 30-38. 

Astrocytes activated by incubation with lipopo-lysaccharide/interferon y for 18 h, induced nitric oxide synthase and, hence, continuously released nitric oxide (Bolanos et al. 1996). coincubation for 24 h of activated astrocytes with neurones caused a limited loss of complex IV activity and had no effect on the activity of complexes I or II-III. However, neurones exposed to astrocytes had a 1.7-fold increase in glutathione concentration compared to neurones cultured alone. Under these coculture conditions, the neuronal ATP concentration was modestly reduced (14 %). This loss of ATP was prevented by the nitric oxide synthase inhibitor, N -monomethyl-L-arginine. 

This cytokine has been shown to play a central role in the neuronal reaction following nerve injury. It is closely involved with microglial and astrocytic activation and neuropeptide expression. There is significant information that indicates that IL-6 is intimately connected to the development of neuropathic pain after peripheral nerve injury. Also, intrathecal administration of IL-6 induces tactile allodynia and thermal hyperalgesia in rats. 

Shrestha, R., Millington, O., Brewer, J., et al., 2014. Lymphocyte-mediated neuroprotection in in vitro models of excitotoxicity involves astrocytic activation and the inhibition of MAP kinase signalling pathways. Neuropharmacology 76 (Pt A), 184-193. 

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