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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuroprotective effect of nerve growth factor (NGF) on the pyramidal cells in the vulnerable CA1-CA2 sectors of the hippocampus was investigated in a rat model of transient forebrain ischemia. A genetically modified fibroblast line that secretes high levels of NGF was implanted 7 days before induction of ischemia between the hippocampal CA1-CA2 subfields in the right hemisphere. Rats were then subjected to 10 min of cerebral ischemia in a four vessel occlusion model. Morphological changes in the CA1 and CA2 subfields were evaluated 7 days after ischemia. Animals in the NGF-protected group had significantly higher numbers of normal appearing neurons in the right CA1 and CA2 regions, compared with their non-implanted left hemispheres, to non-implanted animals or to animals implanted with non-modified cells. The data confirmed that NGF can protect CA1-CA2 hippocampal neurons from ischemic damage by implantation of genetically engineered cells producing NGF.
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PMID:Genetically modified fibroblasts producing NGF protect hippocampal neurons after ischemia in the rat. 760 24

The effect of focal cerebral ischemia induced by middle cerebral artery occlusion on hippocampal interneurons containing the calcium-binding protein parvalbumin (PV) was studied in rats. Four hours after the onset of ischemia, a reduced number of PV-immunoreactive (-ir) neurons was observed in the lateral part of the CA1 region, while PV-ir was not altered in the CA2 and CA3 areas. Pretreatment with the L-type Ca2+ channel blocker nimodipine prevented the ischemia-induced loss of PV-ir in the CA1, suggesting a role for L-type voltage sensitive calcium channels in the mechanism of early neuronal alterations in the hippocampus CA1 region after focal cerebral ischemia.
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PMID:Nimodipine prevents early loss of hippocampal CA1 parvalbumin immunoreactivity after focal cerebral ischemia in the rat. 775 91

Modified four-vessel occlusion in rats caused loss of the passive avoidance response (PAR) and impaired the radial maze performance (RMP). We investigated the effectiveness of bifemelane hydrochloride (bifemelane) in restoring these abilities. After the RMP test, the hippocampal neuronal density following cerebral ischemia was observed histologically and the effect of bifemelane on it examined. Bifemelane was intraperitoneally administered at a dose of 1, 3, 10 mg/kg or 30 mg/kg twice before ischemia and daily following cerebral ischemia. The control rats were given physiological saline in the same manner. At a dose of 10 mg/kg, i.p., bifemelane significantly restored the PAR, which had been lost as a result of 5-min ischemia. At the same dose, it significantly restored the RMP, which had been impaired by 15-min ischemia and prevented neuronal damage in the CA2 region of the anterior hippocampus and the CA1, CA2 and CA3 regions of the posterior hippocampus. The correlation between the memory score and the neuronal density in the CA1 region of the posterior hippocampus was statistically significant. These results suggest that bifemelane might prevent the neuronal damage induced by ischemia and restore impaired learning and memory capabilities following cerebrovascular disease.
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PMID:[Effect of bifemelane hydrochloride in rats on the improvement of the learning and memory impairments and prevention of neuronal damage following transient forebrain ischemia]. 785 20

The effect of (S)alpha-fluoromethylhistidine (FMH), a specific inhibitor of histamine synthesis from histidine, on ischemic damage was examined in gerbil brain after forebrain ischemia. Two h after subcutaneous FMH injection, the histamine content of the brain was significantly reduced. Neuronal loss in the CA2 region of the hippocampus 7 days after 3 min ischemia was enhanced by treatment with FMH. These results indicate that depletion of brain histamine aggravates neuronal death of hippocampal CA2 neurons after 3 min ischemia.
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PMID:Histamine depletion in brain caused by treatment with (S)alpha-fluoromethylhistidine enhances ischemic damage of gerbil hippocampal CA2 neurons. 788 40

In the normal developing hippocampus of the gerbil, parvalbumin-immunoreactive neurons first appear in the stratum pyramidale of CA3 at postnatal day 15 (P15), and in CA2 and hilus of the dentate gyrus from P21 onwards. Immunoreactive terminals also follow the same sequence from CA3 to CA1 to reach adult patterns by the end of the 1st month. Calbindin D-28k immunoreactivity is seen in the external part of the upper blade of the dentate gyrus at P5, and progresses to the granule cell and molecular layers of the whole gyrus by P15, except for a thin band of immature cells located at the base of the granule cell layer which are calbindin negative. Calbindin immunoreactivity in mossy fibers progresses from the external to the hilar region of CA3 during the same period. A few immunoreactive cells are also found in the stratum radiatum/lacunare of the CA3, but no calbindin-immunoreactive cells are observed in the CA1 and CA2 subfields. The adult pattern of calbindin immunoreactivity is reached at P21. Vulnerability following transient forebrain ischemia for 20 min was examined in the hippocampal formation of gerbils during postnatal development. No cellular damage was seen in animals aged 7 days. Dying cells were observed at the base of the granule cell layer of the dentate gyrus in animals aged 15, 21 and 30 days. Pyramidal cells in the CA3 subfield were also sensitive to ischemia in gerbils aged 15 days, and less frequently in animals aged 21 days. The adult pattern of cellular damage, characterized by selective vulnerability of the CA1 subfield, was seen from day 30 onwards.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Poor correlation between delayed neuronal death induced by transient forebrain ischemia, and immunoreactivity for parvalbumin and calbindin D-28k in developing gerbil hippocampus. 794 74

The effect of ischemia-induced hippocampal neuronal damage on acquisition and performance in the Morris water maze task was investigated in male Wistar rats, subjected to 8 min of transient forebrain ischemia, induced by the 4-vessel occlusion (4-VO) method. After a morphological scoring of the neuronal damage within the CA1, CA2, and CA3 subfields of the anterior-dorsal part of hippocampus we found that rats with a total neuronal cell loss of the anterior-dorsal CA1 region showed memory performance impairments in the acquisition trials, in a probe trial, and in a reversal experiment. However, rats with only partial damage to the CA1 region did not exhibit significant impairments during the acquisition trials of the water maze test or in the probe trial and the reversal experiment. In conclusion, these results suggest that it is possible to relate the histological damage score of CA1 in the anterior-dorsal hippocampus to impaired memory performance in the present water maze setup.
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PMID:Does neuronal damage of CA1 relate to spatial memory performance of rats subjected to transient forebrain ischemia? 803 Apr 2

In situ hybridization and Northern blot analysis were used to characterize the mRNA expression of alpha-tubulin, a neuroprotein crucial for neuronal structural and functional restoration, in comparison to that of the stress inducible heat shock protein-70 (HSP-70), in the same gerbil brain following 10 min of forebrain ischemia. The HSP-70 expression was noted in the dentate granule layer 1 h postischemia (PI) and became prominent in all pyramidal cell fields of the hippocampus in addition to the dentate layer at 6 h PI. The induction of HSP-70 persisted in CA1 and CA2 regions and partly in dentate gyrus for up to the 1 day PI period examined. There was no significant HSP-70 expression in any of the regions of the nonischemic or 15 min PI brain. alpha-Tubulin, on the other hand, was expressed in all pyramidal fields of the hippocampus as well as dentate gyrus in nonischemic controls. A decline was noted in the CA1 region 1 h PI onward and was maximal at 6 h PI. Its expression, however, increased at 24 h PI (significant only in comparison to 15 min and 6 h PI but not to control) when it became rather strong in the dentate gyrus. Thus, the temporal pattern of expression of alpha-tubulin sharply contrasted with that of HSP-70 in the PI brain as it declined in the vulnerable CA1 region during the 1st 24 h PI, i.e., the period when HSP-70 was induced and its expression was lowest in the 6 h group when HSP-70 peaked. It was maximum in the dentate gyrus at 24 h PI when HSP-70 was marginally detectable in that region. These studies indicate that in early recirculation period following prolonged ischemia, HSP-70 mRNA is expressed in both vulnerable regions as well as in regions of the brain that are destined to survive while alpha-tubulin is diminished in vulnerable regions. These data suggest a positive correlation between the loss of alpha-tubulin mRNA and delayed neuronal necrosis that follows in the vulnerable CA1 region.
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PMID:Comparison of alpha-tubulin mRNA and heat shock protein-70 mRNA in gerbil brain following 10 min of ischemia. 825 74

Changes in nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 messenger RNA expression in the rat hippocampus following 20 min of transient forebrain ischemia were evaluated using Northern blot analysis and in situ hybridization histochemistry. Twelve hours after the insult, the level of nerve growth factor messenger RNA increased markedly in the granular cell layer of the dentate gyrus and by day 2 returned to control levels. The level of brain-derived neurotrophic factor messenger RNA showed a persistent and moderate increase. The highest expression of brain-derived neurotrophic factor messenger RNA was seen in the dentate granule cells on day 2 after the insult, and then the expression returned to the control levels. At 2 days post-ischemia, contents of messenger RNAs for nerve growth factor and brain-derived neurotrophic factor were reduced in the CA1 region, which may represent delayed loss of vulnerable CA1 pyramidal neurons. In contrast to brain-derived neurotrophic factor and nerve growth factor messenger RNA expression, the level of neurotrophin-3 messenger RNA declined in the CA1, the CA2 and the dentate granular layer immediately after ischemic insult. In the CA1 region, the reduced expression persisted for at least seven days, but in the dentate gyrus, neurotrophin-3 messenger RNA expression returned to the control levels after two days of post-ischemic recovery. These results suggest that nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 genes are differentially regulated and that each of their gene products may play different roles in the central nervous system under pathophysiological conditions.
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PMID:Coordinated expression of messenger RNAs for nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 in the rat hippocampus following transient forebrain ischemia. 835 Sep 88

Following brief cerebral ischemia, tolerance to subsequent ischemia is induced in the hippocampal neurons. In this experiment, recovery of protein synthesis was investigated autoradiographically in gerbils with induced tolerance. The animals were subjected to single forebrain ischemia for 5 min (5-min ischemia group) or 2 min (2-min ischemia group). To observe the effect of tolerance acquisition, double forebrain ischemia (double ischemia group), 2-min ischemia followed by 5-min ischemia was induced 2 days later. At various recirculation periods (90 min, 6 h, 1 day, and 4 days following ischemia), animals received a single dose of L-[2,3-3H]valine. In the 5-min ischemia group, protein synthesis in the CA1 sector was severely suppressed during the period from 90 min to 1 day of recirculation and never returned to the normal level even at 4 day of recirculation. In the 2-min ischemia group, protein synthesis recovered gradually and returned to near normal at 4 days of recirculation. On the other hand, in the double ischemia group, recovery of protein synthesis in the CA1 sector was rapid. At 1 day of recirculation, protein synthesis returned to near normal. Protein synthesis in the CA2 sector was inhibited during the 4 days of recirculation in this group. The present study revealed an early recovery of protein synthesis in the hippocampal CA1 neurons in the gerbil with induced tolerance. We suggest that recovery of protein synthesis is essential for the survival of neurons exposed to transient ischemia.
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PMID:Early recovery of protein synthesis following ischemia in hippocampal neurons with induced tolerance in the gerbil. 837 36

The protective effect on ischemic hippocampal damage was compared between intra- and postischemic hypothermia in Mongolian gerbils and its regional preference was evaluated. Male Mongolian gerbils were subjected to transient forebrain ischemia and the hippocampus 7 days after ischemia was examined histologically. In the intraischemic hypothermia (29-31 degrees C) group, CA1 damage was completely prevented in spite of spontaneous postischemic hyperthermia. In contrast, the same degree of brief postischemic hypothermia exerted no preventive effect. While neurons in the subiculum and CA2 sector were also protected against ischemic damage by intraischemic hypothermia, injured pyramidal neurons were always seen in the CA4 sector.
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PMID:Hypothermic prevention of the hippocampal damage following ischemia in Mongolian gerbils comparison between intraischemic and brief postischemic hypothermia. 844 93


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