Hyperglycemia and acidosis are the hallmarks of diabetes. Since these factors play an important role in diabetic complications, we have studied the brain catecholamine levels in hyperglycemic and acidotic conditions per se. Experimentally induced hyperglycemia and acidosis are accompanied by significant alterations in the catecholamine levels in discrete areas of the brain. We and others have shown that chronic or acute diabetes in animals, as well as in humans results in altered neurotransmitter levels. In the present study, hyperglycemia maintained by daily external administration of glucose for thirty days showed increased level of dopamine in striatum and hippocampus, elevation of norepinephrine in hippocampus, and increased level of epinephrine in hypothalamus, midbrain and pons medulla. The ammonium chloride induced acidosis demonstrated significant elevation of dopamine in midbrain and significant increase of norepinephrine in hypothalamus and midbrain, and increased level of epinephrine in hypothalamus, pons medulla and cerebral cortex. On the other hand, sodium acetoacetate induced acidosis did not show any significant change in the level of catecholamines in any of the areas studied. In conclusion, the changes in catecholamine levels observed in experimentally induced hyperglycemic as well as in acidotic conditions are closely related to the changes observed in spontaneous or alloxan or streptozotocin diabetic animals, thereby suggesting that these conditions may be responsible for the changes observed in diabetic animals.