Activation of dopamine D1 receptors or alpha 1 adrenoceptors is not involved in the EEG effect of nicotine in rats.

Based on previous own EEG-studies and behavioural studies of other authors, it has been claimed recently that D1 receptors are involved in addictive properties of drugs. It seemed, therefore, of interest to study whether nicotine produces D1-characteristic EEG alterations in rats. EEG was recorded in non-anesthetized, freely moving rats, transmitted telemetrically and underwent power spectral analysis. Nicotine (0.1, 0.2, 0.4 mg/kg s.c.) produced a desynchronization in the EEG and a decrease of power in all of the frequency bands (delta, theta, alpha 1, alpha 2, beta 1) except in beta 2. With regard to behaviour, an increase of locomotor activity and some discontinuous sniffing was manifest. The effect of nicotine (0.2 mg/kg) was not antagonized by blockade of dopamine D1 receptors by SCH 23390 (0.1 mg/kg s.c., 30 min before nicotine), although this drug by itself increased the power in most of the frequency bands. Prazosine (0.2 mg/kg i.p.), a selective antagonist at alpha 1 adrenoceptors, by itself increased the power in all of the frequency bands, but also failed to antagonize the effects of nicotine (0.2 mg/kg). In contrast, the blocker of nicotinic cholinoceptors mecamylamine (1 mg/kg i.p.) was effective in antagonizing the action of nicotine on the EEG. The results suggest that in nicotine-mediated desynchronization and decrease of power in the EEG, the activation of dopamine D1 or alpha 1 adrenoceptors is not involved.