Central monoamine dysfunction in diabetes: psychotherapeutic implications: electroanalysis by voltammetry.

The effects of chemically, i.e., streptozotocin-induced diabetes or induced hyperglycemia on dopamine and serotonin release in striatum were examined in vivo in rats by employing voltammetry. In the acutely diabetic state, an increased (67%) striatal dopamine release was seen, whereas in the chronically diabetic state, striatal dopamine release was increased, but not to the same extent (19%). The acutely diabetic rat, in which electrochemical signals for serotonin were studied 3 days after the single intraperitoneal injection of STZ, responded with a significant increased release of serotonin (62%). Chronically diabetic rats showed a reversal of serotonin release to basal values. When L-tryptophan was injected in nondiabetic rats, the results showed a decrease (45%) in striatal dopamine release. Injection of L-tryptophan into nondiabetic rats produced a significant increase (25%) over control values in the striatal release of serotonin. The maximum increase was most evident 90 min after injection and the increase remained elevated an additional 90 min. Long term diabetic animals showed a significant decrease (73%) in striatal dopamine release after L-tryptophan. Long term diabetes produced a significant inhibition of serotonin release over control values to 70% below baseline levels. The effects of hyperglycemia on non-diabetic rats were a decreased (52%) striatal dopamine release and an increased (304%) striatal serotonin release. These changes imply that the untreated diabetic state is associated with progressive impairment of neurotransmitter release. These data can be interpreted as implying that mood changes may be related to impaired neurotransmitter availability in the diabetic state.