IN-UTERO COCAINE EXPOSURE DECREASES DOPAMINE D1 RECEPTOR MODULATION OF HIPPOCAMPAL LONG-TERM POTENTIATION IN THE RABBIT

Cocaine increases the synaptic concentration of neurotransmitters by i nhibiting catecholamine transporters. Disturbances of behavior and cel lular physiology have been associated with prenatal cocaine exposure a nd are related to changes in dopamine transmission. Recently we found the magnitude of long-term potentiation (LTP) was greater in hippocamp al slices from cocaine exposed offspring. In the hippocampus, D1 dopam ine receptor antagonists inhibit the expression of LTP while agonists facilitate it. To test the functionality of the D1 receptor we examine d the effect of the D1 antagonist SCH-23390 on LTP using a rabbit mode l of gestational cocaine exposure. Tetanization during exposure to the D1 antagonist SCH-23390 resulted in a long lasting potentiation in an imals prenatally exposed to cocaine while the potentiation of control slices returned to baseline.