Short communicationTransport of fragmented DNA in apical dendrites of gerbil CA1 pyramidal neurons following transient forebrain ischemia
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Acknowledgements
The authors wish to thank Kyoko Takahashi, Chikako Usui and Kimiko Nakamura for technical assistance.
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Exercise training attenuates cerebral ischemic hyperglycemia by improving hepatic insulin signaling and β-cell survival
2013, Life SciencesCitation Excerpt :Transient cerebral ischemia following unilateral common carotid artery occlusion in gerbils leads to delayed neuronal degeneration of several brain regions, including the hippocampus, and is similar to carotid artery occlusion in humans (Matsumoto et al., 1990; Horn and Schlote, 1992). Many studies have indicated that the post-ischemic DNA fragmentation in the hippocampal CA1 area in experimental ischemic models is a key phenomenon for the delayed neuronal death (Hara et al., 1998a). Most studies have shown that 5 min of carotid artery occlusion in gerbils produces neuronal damage in the hippocampus, cerebral cortex and striatum (Matsumoto et al., 1987; Janac et al., 2006).
Pre-administration of L-tryptophan improved ADR-induced early renal failure in mice
2012, Life SciencesCitation Excerpt :Secondary antibodies used were VECTASTAIN kit (VECTOR LABORATORIES) anti-mouse or rabbit IgG antibody. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method was performed as described previously (Hara et al., 1998) with some modifications to the method as suggested by Gavrieli et al. (Gavrieli et al., 1992). After incubation with 20 mg/ml proteinase K (Sigma), the serial sections used for HE staining were immersed in TDT buffer (30 mM Trizma base, pH 7.2, 140 mM sodium cacodylate, 1 mM cobalt chloride).
Galectin-3 expression in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia, and its inhibition by hypothermia
2011, Brain ResearchCitation Excerpt :Furthermore, a brief episode of ischemia causes “delayed neuronal death” in the CA1 sector of the hippocampus (Kirino, 1982). Accumulating evidence has indicated that the post-ischemic DNA fragmentation in the hippocampal CA1 area in experimental ischemic models is a key phenomenon for the delayed neuronal death and is considered as apoptosis (Heron et al., 1993; Iwai et al., 1995; Hara et al., 1998a). Although many studies have shown the underlying mechanisms related to delayed neuronal death after transient ischemia, exact mechanisms are not yet fully understood.
Localization and spatiotemporal expression of IDO following transient forebrain ischemia in gerbils
2008, Brain ResearchCitation Excerpt :In the present study, double immunofluorescence detections of IDO and NeuN, and IDO and GFAP, which were performed in hippocampal CA1 sector clearly showed that the source of expressed IDO, at least in the CA1 region, is not from astrocytes but from neurons. Recently, many studies support the hypothesis that delayed neuronal death of the CA1 pyramidal neurons after transient forebrain ischemia is not necrotic but apoptotic (Hara et al., 1998a). Morphological and biochemical data, such as DNA fluorescence assay, in situ nick-end-labeling method, gel electrophoresis and electron microscopy, indicate that delayed neuronal death is a form of programmed cell death, or apoptosis.
Suppression of hyperemia and DNA oxidation by indomethacin in cerebral ischemia
2003, European Journal of Pharmacology