Reaction of astrocytes in the gerbil hippocampus following transient ischemia: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase, and S-100 protein
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2024, Journal of Stroke and Cerebrovascular DiseasesGenomic approach to selective vulnerability of the hippocampus in brain ischemia-hypoxia
2015, NeuroscienceCitation Excerpt :Taken together, the difference between CA1 and CA3 is relative, and it is observed after short periods of ischemia, as would occur in cardiac arrest with survival under clinical conditions. Numerous studies have used immunohistochemical markers for astrocytes and microglial cells after global brain ischemia (Petito et al., 1990; Schmidt-Kastner et al., 1990; Morioka et al., 1991, 1992; Tanaka et al., 1992; Jørgensen et al., 1993; Ordy et al., 1993; Sugawara et al., 2002). As a simplification, the response of astrocytes and microglial cells in CA1 starts early after ischemia and becomes prominent when neurons become necrotic.
Severity of middle cerebral artery occlusion determines retinal deficits in rats
2014, Experimental NeurologyCitation Excerpt :By 9 days post-MCAO, GS levels returned to normal, suggesting that GS may clear all of the excess glutamate and allow for recovery of retinal function. Similarly, increases in GS have been observed from 3 h to 3 days after cerebral ischemia (Hoshi et al., 2006; Petito et al., 1992; Tanaka et al., 1992; Verma et al., 2010), and these increases appear to be transient, returning to baseline levels by 5 days (Tanaka et al., 1992). Additionally, treatments that enhance the activity of glutamate transporter (Verma et al., 2010) and GS (Zhang et al., 2011) have been shown to reduce brain injury in ischemia-reperfusion models, providing further support for a protective role of GS in reducing levels of extracellular glutamate after ischemic injury.
L-3-n-butylphthalide improves cognitive deficits in rats with chronic cerebral ischemia
2012, Neuropharmacology