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1996 | 56 | 1 | 41-48
Article title

Changes of Ca2+/calmodulin - dependent protein kinase-II after transient ischemia in gerbil hippocampus

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EN
Abstracts
EN
Transient cerebral ischemia induces, besides delayed neurodegeneration in selected brain structures, a number of early responses which may mediate ischemic injury/repair processes. Here we report that 5 min exposure to cerebral ischemia in gerbils induces a rapid inhibition and subsequent translocation of Ca (2+)/calmodulin-dependent protein kinase II (CaMKII). These changes were partially reversible during a 24 h post-ischemic recovery. Concomitantly the total amount of the enzyme protein, as revealed by Western blotting (alfa- -subunit specific), remained stable. This is consistent with our previous hypothesis, that the mechanism of ischemic CaMKII down-regulation involves a reversible posttranslational modification-(auto)phosphorylation, rather then the degradation of enzyme protein. The effectiveness of known modulators of postischemic outcome in counteracting CaMKII inhibition was tested. Three of these drugs, namely dizocilpine (MK-801), N-nitro-L-arginine methyl ester (L-NAME) and gingkolide (BN52021), all significantly attenuated the enzyme response to ischemia, whereas an obvious diversity in the time-course of their actions implicates different mechanisms involved.
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Year
Volume
56
Issue
1
Pages
41-48
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proceeding
Publication order reference
T.Zalewska
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YADDA identifier
bwmeta1.element.element-from-psjc-8c00c1e2-a0df-37e4-8b70-95a4eff5706b
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