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Cited by (36)
Genomic approach to selective vulnerability of the hippocampus in brain ischemia-hypoxia
2015, NeuroscienceCitation Excerpt :Given the difficulty to delineate CA2 in ischemic damage (Akai and Yanagihara, 1993) no specific discussion of CA2 will be provided in the remainder of the review. At the medial border of CA1, the transition of damage to the subiculum is not well studied (Akai and Yanagihara, 1993). Hilar neurons (“CA4”) are very vulnerable, and the somatostatin expressing subclass seems to be rapidly affected (Johansen et al., 1987).
PPAR-γ activator induces neuroprotection in hypercholesterolemic rats subjected to global cerebral ischemia/reperfusion injury: In vivo and in vitro inhibition of oxidative stress
2014, Experimental GerontologyCitation Excerpt :Global cerebral ischemia/reperfusion injury (GCI/R) occurs in conditions like cardiac arrest, coronary artery bypass surgery, cardio-respiratory failure, and others leading to drastic reduction of blood flow to the brain (Llinas et al., 2000). Global cerebral ischemia, for a short period of time, results in selective neuro-degeneration in vulnerable brain areas, such as CA1 region of the hippocampus (Akai and Yanagihara, 1993; Pulsinelli 1995). The underlying mechanisms of CA1 neuronal loss following GCI/R may involve reactive oxygen species (ROS), inflammation, and apoptosis (Ferrer and Plana, 2003; Wang et al., 2007).
Neuroprotective effect of melatonin on brain damage induced by acute global cerebral ischemia in cats
2001, Archives of Medical Research