Hyperglycemia and
acidosis are the hallmark of diabetes. Since these factors play an important role in the
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 human 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.