BIOCHEMICAL-STUDIES SUPPORT THE ASSUMPTION THAT DOPAMINE PLAYS A MINOR ROLE IN THE EEG EFFECTS OF NICOTINE

In a previous study, it was shown that a moderate dose of nicotine (0. 2 mg/kg SC) produced a desynchronization in the EEG and a decrease of power which was not antagonized by blockade of D-1-like dopamine recep tors, although this EEG pattern seemed to be characteristic for activa tion of D-1-like rather than D-2-like receptors. This seemed surprisin g, since nicotine is known to enhance dopaminergic neurotransmission i n the basal ganglia. Since there is a strong reciprocal connection bet ween the cortex and the striatum, dopaminergic effects on the striatum should lead to alterations in the cortical EEG. Therefore: the releas e of dopamine was studied in the striatum by using microdialysis in aw ake rats, and in parallel studies, the EEG was studied after administr ation of a larger dose of nicotine (0.4 mg/kg SC). This is a dose whic h does not induce toxic side effects. This dose produced a desynchroni zation in the EEG and a decrease of power. The increase in extracellul ar dopamine in the striatum was very moderate (by about 30%) and of sh orter duration than the EEG effect. Therefore, activation of striatal dopaminergic neurotransmission does not seem to be relevant for the EE G effect studied.