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 s.c.) produced a desynchronization in the EEG and a decrease of power which was not antagonized by blockade of D1-like dopamine receptors, although this EEG pattern seemed to be characteristic for activation of D1-like rather than D2-like receptors. This seemed surprising, since nicotine is known to enhance dopaminergic neurotransmission in the basal ganglia. Since there is a strong reciprocal connection between the cortex and the striatum, dopaminergic effects on the striatum should lead to alterations in the cortical EEG. Therefore, the release of dopamine was studied in the striatum by using microdialysis in awake rats, and in parallel studies, the EEG was studied for administration of a larger dose of nicotine (0.4 mg/kg s.c.). This is a dose which does not induce toxic side effects. This dose produced a desynchronization in the EEG and a release of power. The increase in extracellular dopamine in the striatum was very moderate (by about 30%) and of shorter duration than the EEG effect. Therefore, activation of striatal dopaminergic neurotransmission does not seem to be relevant for the EEG effect studied.