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

• Authors: T. Zalewska , B. Zablocka , K. Domanska-Janik
• Languages of publication: 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.

Keywords

EN

BRAIN ISCHAEMIA; NEUROPROTECTION

Discipline

• EXPERIMENTAL_BIOLOGY_&_MEDICINE: EXPERIMENTAL BIOLOGY & MEDICINE

• Publisher: Marceli Nencki Institute of Experimental Biology, Polish Academy of Sciences
• Journal: Acta Neurobiologiae Experimentalis
• Year: 1996
• Volume: 56
• Issue: 1
• Pages: 41-48

Contributors

author

T. Zalewska

author

B. Zablocka

author

K. Domanska-Janik

• Document Type: proceeding
• Publication order reference: T.Zalewska