Studies on electroencephalogram (EEG) in rats suggest that moderate doses of cocaine or d-amphetamine activate D1 rather than D2 receptors.

The effects of cocaine and d-amphetamine, two psychomotor stimulant drugs with pronounced addictive properties, on the electroencephalogram (EEG) of rats were studied by telemetric recordings from the skull in non-anesthetized, freely moving rats. The electrocorticogram (ECoG) was recorded. Both cocaine (10 mg/kg IP) and d-amphetamine (0.4 mg/kg IP) produced a desynchronization, characterized by a general lowering in power in all of the frequency bands. These effects of both drugs were mimicked by the selective agonist at D1 receptors SK&F 38393 (3 mg/kg SC) and were reversed by the antagonist at D1 receptors SCH 23390 (0.2 mg/kg IP) but not influenced by haloperidol (0.1 mg/kg IP) in a dose which is likely to block D2 rather than D1 receptors. These doses of cocaine or d-amphetamine did not produce stereotyped behaviour and slight, if any, increases in locomotor activity only. Large doses of cocaine (30 mg/kg IP) or d-amphetamine (4 mg/kg IP) produced stereotyped behaviour and alterations in EEG which are, based on previous own studies, characteristic for additional stimulation of D2 receptors. This was manifest in a selective increase in power of the alpha-1 band. A similar effect was also produced by the agonist both at D1 and D2 receptors, apomorphine (0.5 mg/kg SC). These results suggest that moderate, but probably rewarding doses of cocaine or d-amphetamine mainly activate D1 dopamine receptors. This activation might be relevant for the rewarding properties of these drugs.