Stressor specificity and effect of prior experience on catecholamine biosynthetic enzyme phenylethanolamine...

The specific activation of two components of the sympathoadrenal system (adrenomedullary and sympathoneural) by various stressors was recently described. The aim of this work was to investigate changes in catecholamine (CA) biosynthetic enzyme phenylethanolamine N-methyltransferase (PNMT) gene expression, protein level, and activity in the adrenal medulla of rats after a single or repeated exposure to various homotypic or novel heterotypic stressors. Immobilization for 2 h (IMO), cold 4 degrees C (COLD), administration of insulin 5I U (INS), or 2-deoxyglucose 500 mg/kg (2DG) were used as stressors. Plasma epinephrine (EPI) and norepinephrine (NE) levels clearly showed that these stressors specifically activate the aforementioned systems. A single exposure to IMO, COLD, INS, or 2DG induced increases in PNMT mRNA levels in the adrenal medulla. Besides PNMT mRNA, repeated exposure to IMO also elevated activity and protein levels of the enzyme; however, chronic cold exposure did not show PNMT changes compared to control animals at room temperature. PNMT gene expression was also investigated in rats adapted to repeated immobilization stress or to chronic cold exposure after a single exposure to various heterotypic novel stressors. Cold-adapted rats responded to heterotypic novel stressors (IMO, INS) by exaggerated responses of PNMT mRNA levels compared to responses in naive rats exposed to the same stressors at room temperature. Immobilization-adapted rats did not show exaggerated responses of PNMT mRNA after exposure to novel stressors. Therefore, observed differences in plasma CA and adrenomedullary mRNA levels suggest a specific regulation of CA release, synthesis, and gene expression of CA biosynthetic enzymes, which depends on the quality of the stressor. Exposure of adapted rats to novel stressors induces exaggerated responses, but this process also depends on the specificity of the stressor used. Different stressors regulate PNMT gene expression by specific mechanisms especially in chronically stressed rats. These mechanisms remain to be elucidated. It is the ability of the long-term stressed organism to respond differently to novel heterotypic stressors that we consider an important adaptive phenomenon of catecholaminergic systems in rats.