Concurrent elicitation of electroencephalographic desynchronization and penile erection by cocaine in the rat.

It is well-known from animal and human studies that, as a central nervous stimulant, cocaine induces electroencephalographic (EEG) desynchronization. Cocaine also purportedly increases sexual behavior as an aphrodisiac. Whether the effects of cocaine on EEG activity and penile erection are mechanistically linked, however, remains to be fully elucidated. We evaluated whether this link exists, based on simultaneous recording of EEG signals from the somatosensory cortex and intracavernous pressure (ICP, as experimental index for penile erection) in adult, male Sprague-Dawley rats. Under intraperitoneal chloral hydrate anesthesia (400 mg/kg, i.p.), both intravenous (i.v.) and intracavernous (i.c.) administration of cocaine (1.5 or 3.0 mg/kg, and 75 or 150 micrograms) dose-dependently induced discernible EEG desynchronization, as represented by a decrease in root mean square and an increase in mean power frequency values, and an increase in ICP. However, the same administration of cocaine in animals under pentobarbital sodium anesthesia (50 mg/kg, i.p.) failed to significantly affect EEG activity, despite an appreciable dose-dependent elevation in ICP. On the other hand, intracerebroventricular administration of cocaine (7.5, 15, or 30 micrograms) induced significant EEG activation without affecting ICP. I.c. application of papaverine (400 micrograms) elicited a discernible increase in ICP, but failed to evoke EEG desynchronization. These results suggest that the concurrent EEG desynchronization and penile erection elicited by cocaine may take place without a mutually causative relationship.