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 receptors, although this EEG pattern seemed to be characteristic for activation of D-1-like rather than D-2-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 after administration of a larger dose of nicotine (0.4 mg/kg SC). This is a dose which does not induce toxic side effects. This dose produced a desynchronization in the EEG and a decrease 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.