Differential activation of JNK in rat hippocampus following acute and/or chronic stressors.

Abstract

c-Jun N-terminal kinase (JNK) is activated by phosporylation in response to cellular stressors and extracellular signals and plays a role in the activation of glucocorticoid receptor (GR) and contributes to the stress-induced apoptosis. Therefore, the expression protein pattern of the active forms of cytosolic phospho- JNK (P-JNK) and inactive JNK in hippocampus of rats exposed to 21daily isolation as chronic stressor, sole and in combination with 2hrs acute stressors of immobilization (IM) or cold (4oC), were followed by Western blot. Concentration of serum corticosterone was monitored. We found significant increase in the levels of P-JNK following acute IM. Decreased levels of P-JNK following chronic isolation and when isolation preceded the application of acute IM were found, compared to its level after acute IM. Data suggest that diminished expresion of PJNK level following chronic isolation in hippocampus, might be involved in deregulation of intracellular GR negative feedback control as well as stress-induced apoptosis.Physical chemistry 2008 : 9th international conference on fundamental and applied aspects of physical chemistry; Belgrade (Serbia); 24-28 September 200

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