ACTIVATION OF DOPAMINE D-1 RECEPTORS OR ALPHA(1) ADRENOCEPTORS IS NOTINVOLVED IN THE EEG EFFECT OF NICOTINE IN RATS

Based on previous own EEG-studies and behavioural studies of other aut hors, it has been claimed recently that D-1 receptors are involved in addictive properties of drugs. It seemed, therefore, of interest to st udy whether nicotine produces D-1-characteristic EEG alterations in ra ts. EEG was recorded in non-anesthetized, freely moving rats, transmit ted 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 man ifest. The effect of nicotine (0.2 mg/kg) was not antagonized by block ade of dopamine D-1 receptors by SCH 23390 (0.1 mg/kg s.c., 30 min bef ore nicotine), although this drug by itself increased the power in mos t of the frequency bands. Prazosine (0.2 mg/kg i.p.), a selective anta gonist 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 cholinocep tors mecamylamine (1 mg/kg i.p.) was effective in antagonizing the act ion of nicotine on the EEG. The results suggest that in nicotine-media ted desynchronization and decrease of power in the EEG, the activation of dopamine D-1 or alpha(1), adrenoceptors is not involved.