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 inhibiting catecholamine transporters. Disturbances of behavior and cellular physiology have been associated with prenatal cocaine exposure and are related to changes in dopamine transmission. Recently we found the magnitude of long-term potentiation (LTP) was greater in hippocampal slices from cocaine exposed offspring. In the hippocampus, D1 dopamine receptor antagonists inhibit the expression of LTP while agonists facilitate it. To test the functionality of the D1 receptor we examined the effect of the D1 antagonist SCH-23390 on LTP using a rabbit model of gestational cocaine exposure. Tetanization during exposure to the D1 antagonist SCH-23390 resulted in a long lasting potentiation in animals prenatally exposed to cocaine while the potentiation of control slices returned to baseline.
Neurobiology Department, Northeastern Ohio Universities College of Medicine, Rootstown 44272, USA. jzl@riker.neoucom.edu
J Z
JZ
Little
T J
TJ
Teyler
D000818:Animals; D003042:Cocaine / Q000494:pharmacology*; D005260:Female; D006624:Hippocampus / Q000187:drug effects*; D017774:Long-Term Potentiation / Q000187:drug effects*; D011817:Rabbits; D017447:Receptors, Dopamine D1 / Q000187:drug effects*; D014599:Uterus / Q000187:drug effects*
D017447:Receptors, Dopamine D1; D003042:Cocaine