Protective effect of prior fimbria-fornix deafferentation on hippocampal CA1 following transient forebrain ischemia is mediated by GluR2 expression

Protective effect of prior fimbria-fornix deafferentation on hippocampal CA1 following transient forebrain ischemia is mediated by GluR2 expression

Bibliográfalaš dieđut
Váldodahkkit:	Kaur, J, Zhao, Z, Geransar, R, Sun, P, Buchan, A
Materiálatiipa:	Conference item
Almmustuhtton:	2005

Geahča maid

Prior deafferentation confers long term protection to CA1 against transient forebrain ischemia and sustains GluR2 expression.
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Almmustuhtton: (2006)

Neuroprotection and neurogenesis: modulation of cornus ammonis 1 neuronal survival after transient forebrain ischemia by prior fimbria-fornix deafferentation.
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Fimbria/Fornix deafferentation protects CA1 neurons and enhances neurogenesis in hippocampus following global ischemia
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Hypothermia rescues hippocampal CA1 neurons and attenuates down-regulation of the AMPA receptor GluR2 subunit after forebrain ischemia.
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Septo-hippocampal deafferentation protects CA1 neurons against ischemic injury.
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Erythropoietin Improves Place Learning in an 8-Arm Radial Maze in Fimbria-Fornix Transected Rats
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Indefatigable CA1 sector neuroprotection with mild hypothermia induced 6 hours after severe forebrain ischemia in rats.
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A selective N-type Ca(2+)-channel blocker prevents CA1 injury 24 h following severe forebrain ischemia and reduces infarction following focal ischemia.
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Upregulation of AMPA receptor GluR2 (GluA2) subunits in subcortical ischemic vascular dementia is repressed in the presence of Alzheimer's disease.
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The correlation of GluR3B antibody with T lymphocyte subsets and inflammatory factors and their role in the progression of epilepsy
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The N-methyl-D-aspartate antagonist, MK-801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats.
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