An acute hyperglycemia or acidosis-induced changes of indolamines level correlates with PKC-α expression in rat brain

Abstract Hyperglycemia and ketoacidosis are the two most serious factors in acute metabolic complications of both type 1 and type 2 diabetes. Dysfunction of the central nervous system is a well-documented complication of diabetes. We and others have previously reported that acute or chronic diabetes in animal's results in altered brain neurotransmitter levels. In this study, we investigated the effects of acute (7 days) glucose-induced hyperglycemia and sodium acetoacetate (NaAcAc) or ammonium chloride (NH 4 Cl) induced acidosis on the level of indolamines (5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA)) as well as PKC-α expression/activity in discrete areas of rat brain. Glucose-induced (500 mg/kg, bw) hyperglycemic (∼249 mg%) rats showed significant ( p p p p