Profound but transient deficits in learning and memory after global ischemia using a novel water maze test

Euler, Mia von; Bendel, Olof; Bueters, Tjerk; Sandin, Johan; Euler, Gabriel von

doi:10.1016/j.bbr.2005.07.016

Cited by 32 publications

(31 citation statements)

References 24 publications

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“…In addition, many studies have shown that an increased proliferation of neural progenitor cells starts at 3-4 days post-ischemia, peaks at 7-10 days post-ischemia and returns to the control level by 3-5 weeks after global cerebral ischemia (29,47,50,52). However, Bendel and coworkers (37) reported that about 40% of CA1 neurons had reappeared 90 days after transient ischemic insult, whereas some researchers reported that the tertiary cell death had appeared between 90 and 125 days after ischemic damage (3,51). Furthermore, Bueters et al (4) reporetd that newly formed CA1 cells had partly disappeared 250 days after ischemia.…”

Section: Discussionmentioning

confidence: 94%

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New GABAergic Neurogenesis in the Hippocampal CA1 Region of a Gerbil Model of Long‐Term Survival after Transient Cerebral Ischemic Injury

et al. 2015

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We investigated the probability of newly generated neurons that could survive and mature in the ischemic hippocampal CA1 region (CA1) of a gerbil model of transient cerebral ischemia. Neuronal death was shown in the stratum pyramidale (SP) from 4 days post-ischemia, and a significant increase in NeuN-positive ((+) ) neurons was found in the SP at 180 days post-ischemia. 5-Bromo-2-deoxyuridine (BrdU)(+) cells were co-stained with NeuN and glutamic decarboxylase 67 (GAD67). Brain-derived neurotrophic factor (BDNF) immunoreactivity and protein level was shown in nonpyramidal cells from 4 days post-ischemia, and the immunoreactivity was strong at 30 days post-ischemia and not significantly changed until 180 days post-ischemia. Furthermore, TrkB immunoreactivity was co-stained with GAD67 when we examined at 180 days post-ischemia. Myelin basic protein (MBP)(+) nerve fibers were reduced at 4 days post-ischemia and maintained until 60 days post-ischemia, and MBP immunoreactivity and levels were significantly increased at 180 days post-ischemia. In the passive avoidance test, cognitive dysfunction was improved at 180 days post-ischemia. These results suggest that the differentiation of neural progenitor cells into new GABAergic neurons may be promoted via BDNF in the ischemic CA1 and that the neurogenesis may partially mediate the recovery of cognitive impairments via increasing myelinated nerve fibers.

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Section: Discussionmentioning

confidence: 94%

“…Cognitive function in ischemic animals is impaired at 14 days post-ischemia, and the cognitive dysfunction subsides at 90 or 125 days post-ischemia (3,51). In particular, ischemic hippocampal damage leads to cognitive dysfunction as an evident from reduction in response latency in passive avoidance test (17).…”

Section: Discussionmentioning

confidence: 99%

New GABAergic Neurogenesis in the Hippocampal CA1 Region of a Gerbil Model of Long‐Term Survival after Transient Cerebral Ischemic Injury

et al. 2015

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“…The deletion of the CA1 pyramidal neurons is associated with severe impairment of hippocampal-dependent brain functions, including spatial learning ability and short-term memory (4,22,23). Following transient global ischemia in gerbils, short-term memory in the step-down avoidance task is impaired (5).…”

Section: Discussionmentioning

confidence: 99%

Ulinastatin inhibits cerebral ischemia-induced apoptosis in the hippocampus of gerbils

CHO

Shin

et al. 2015

Molecular Medicine Reports

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Ulinastatin is a urinary trypsin inhibitor, originally extracted and purified from human urine. Ulinastatin has cytoprotective effects against ischemic injury in several organs. In the present study, the neuroprotective effects of ulinastatin following ischemic cerebral injury in the hippocampus of gerbils was investigated. To induce transient global ischemia in gerbils, the common carotid arteries were occluded using aneurysm clips for 5 min, and the clips were then removed. Ulinastatin was subcutaneously injected into the gerbils once a day for 7 days at doses of 50,000 or 100,000 U/kg. The gerbils were confronted with a step-down avoidance task, following which tissue samples from the gerbils were examined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, western blot analysis for B-cell lymphoma (Bcl-2) and Bcl-2-associated X protein (Bax), immunohistochemistry for caspase-3 and immunofluorescence for 5-bromo-2′-deoxyuridine. The numbers of TUNEL-positive and caspase-3-positive cells in the hippocampal CA1 region increased following cerebral ischemia. The expression of Bax in the hippocampus increased, while the expression of Bcl-2 in the hippocampus decreased following cerebral ischemia. These results confirmed that apoptosis in the hippocampus was enhanced following cerebral ischemia in gerbils. The levels of cell proliferation in the hippocampal dentate gyrus were also enhanced by ischemia, which is possibly an adaptive mechanism to compensate for excessive levels of apoptosis. Ulinastatin treatment inhibited ischemia-induced apoptosis by suppressing apoptosis-associated molecules, and thus ameliorated ischemia-induced short-term memory impairment. The cell proliferation in the hippocampus was also suppressed following ulinastatin treatment. These results suggested the use of ulinastatin as a therapeutic agent for patients with cerebral stroke.

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“…16 The rat was placed in the water facing the wall at one random start location out of four (north, south, east, and west), located equidistance from one another around the rim of the pool. Each rat was then allowed to find the submerged platform within 90 seconds, and rest on it for 20 seconds.…”

Section: Behavioral Assessment With Morris Water Mazementioning

confidence: 99%

Inhalation of hydrogen gas attenuates cognitive impairment in transient cerebral ischemia via inhibition of oxidative stress

Zhao

et al. 2012

Neurological Research

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Profound but transient deficits in learning and memory after global ischemia using a novel water maze test

Cited by 32 publications

References 24 publications

New GABAergic Neurogenesis in the Hippocampal CA1 Region of a Gerbil Model of Long‐Term Survival after Transient Cerebral Ischemic Injury

New GABAergic Neurogenesis in the Hippocampal CA1 Region of a Gerbil Model of Long‐Term Survival after Transient Cerebral Ischemic Injury

Ulinastatin inhibits cerebral ischemia-induced apoptosis in the hippocampus of gerbils

Inhalation of hydrogen gas attenuates cognitive impairment in transient cerebral ischemia via inhibition of oxidative stress

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