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

Abstract

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.

Changes in sexual function and gonadal axis hormones after switching to aripiprazole in male schizophrenia patients

“…Several lines of evidence in animal and human males support a role of central dopaminergic neurotransmission in mediating sexual behavior and erection (Melis and Argiolas, 1995;Chang et al, 1996;Giuliani, 1996, 1997). The mechanism underlying the improvement in sexual dysfunction after switching to aripiprazole may be associated with dopamine and serotonin transmissions.…”

Hippocampal noradrenergic neurotransmission in concurrent EEG desynchronization and inhibition of penile erection induced by cocaine in the rat

“…As in our previous studies ( Chang et al ., 1994 ; 1995 ; 1996 ; 1998a , 1998b ), EEG signals were recorded bilaterally and differentially with two stainless steel screws implanted epidurally above the primary somatosensory cortex (1 mm posterior to the bregma and 5 mm lateral to the midline). EEG signals from the right side of the hippocampal formation were concurrently recorded via a stereotaxically positioned bipolar concentric electrode (Rhodes Medical SNE‐100, Woodland Hills, CA, U.S.A.) at: 2.3–3.2 mm posterior to the bregma, 3.6–4.4 mm from the cortical surface, 1.5–2.4 mm lateral to the midline ( Chang et al ., 1998a , 1998b ).…”

“…Both cortical and hippocampal (cEEG and hEEG) signals were subject to continuous, on‐line and real‐time spectral analysis ( Chang et al ., 1994 ; 1995 ; 1996 ; 1998a , 1998b ). In particular, we quantified the magnitude of EEG activity by calculating the root mean square (RMS) value.…”

I.v. cocaine induces rapid, transient excitation of striatal neurons via its action on peripheral neural elements: Single-cell, iontophoretic study in awake and anesthetized rats

“…Both chloral hydrate and pentobarbital anesthesia also significantly attenuated or blocked cortical EEG desynchronization (Chang et al 1996) and transient increases in sympathetic nerve discharges (Abrahams et al 1996), other rapid, centrally mediated effects of iv COC seen in awake rats. The latter effect in splanchnic nerve discharges, suggesting transient sympathoexcitation, matched temporally the COC-induced activation of striatal neurons in this study, suggesting a possible common cause.…”