Participation of the cholinergic system in the ethanol-induced suppression of paradoxical sleep in rats.

Sleep disturbance is among the many consequences of ethanol abuse in both humans and rodents. Ethanol consumption can reduce REM or paradoxical sleep (PS) in humans and rats, respectively. The first aim of this study was to develop an animal model of ethanol-induced PS suppression. This model administered intragastrically (by gavage) to male Wistar rats (3 months old, 200-250 g) 0.5 to 3.5 g/kg ethanol. The 3.5 g/kg dose of ethanol suppressed the PS stage compared with the vehicle group (distilled water) during the first 2-h interval (0-2 h; 1.3 vs 10.2; P < 0.001). The second aim of this study was to investigate the mechanisms by which ethanol suppresses PS. We examined the effects of cholinergic drug pretreatment. The cholinergic system was chosen because of the involvement of cholinergic neurotransmitters in regulating the sleep-wake cycle. A second set of animals was pretreated with 2.5, 5.0, and 10 mg/kg pilocarpine (cholinergic agonist) or atropine (cholinergic antagonist). These drugs were administered 1 h prior to ethanol (3.5 g/kg) or vehicle. Treatment with atropine prior to vehicle or ethanol produced a statistically significant decrease in PS, whereas pilocarpine had no effect on minutes of PS. Although the mechanism by which ethanol induces PS suppression is not fully understood, these data suggest that the cholinergic system is not the only system involved in this interaction.

Participation of the cholinergic system in the ethanol-induced suppression of paradoxical sleep in rats

Sleep disturbance is among the many consequences of ethanol abuse in both humans and rodents. Ethanol consumption can reduce REM or paradoxical sleep (PS) in humans and rats, respectively. The first aim of this study was to develop an animal model of ethanol-induced PS suppression. This model administered intragastrically (by gavage) to male Wistar rats (3 months old, 200-250 g) 0.5 to 3.5 g/kg ethanol. The 3.5 g/kg dose of ethanol suppressed the PS stage compared with the vehicle group (distilled water) during the first 2-h interval (0-2 h; 1.3 vs 10.2; P < 0.001). The second aim of this study was to investigate the mechanisms by which ethanol suppresses PS. We examined the effects of cholinergic drug pretreatment. The cholinergic system was chosen because of the involvement of cholinergic neurotransmitters in regulating the sleep-wake cycle. A second set of animals was pretreated with 2.5, 5.0, and 10 mg/kg pilocarpine (cholinergic agonist) or atropine (cholinergic antagonist). These drugs were administered 1 h prior to ethanol (3.5 g/kg) or vehicle. Treatment with atropine prior to vehicle or ethanol produced a statistically significant decrease in PS, whereas pilocarpine had no effect on minutes of PS. Although the mechanism by which ethanol induces PS suppression is not fully understood, these data suggest that the cholinergic system is not the only system involved in this interaction.

Sleep pattern in rats under different stress modalities.

The present study was designed to evaluate the sleep pattern of rats submitted to chronic stressors (restraint, electrical footshock, swimming and cold) applied to male rats. After 48 h-baseline recording, rats were submitted to 4 days of chronic stress, and electrocorticogram recordings were carried out continuously. The stressors (footshock, swimming and cold) were applied twice a day for periods of 1 h at 9:00 and 16:00 h. Restrained animals were maintained in plastic cylinders for 22 h/day. The findings indicated that sleep efficiency, slow wave sleep (SWS) and paradoxical sleep (PS) were decreased on the third and fourth days of unpredictable shocks compared to baseline while immobilization and swimming presented reduced sleep efficiency in all 4-day recordings. Swimming led to decreased SWS, whereas augmented PS was observed on the first day compared to baseline. Immobilization produced drastic alterations in sleep patterns since it reduced SWS during the 4 days and PS at days 1 to 4 in relation to baseline. Of all stressors, cold was the only one that did not result in any statistical differences in sleep pattern during the light periods. Regarding the effect of stress compared to baseline on the dark recordings, PS was higher during cold stress periods, whereas footshock increased PS on days 2 to 4 and swimming only on day 2. Immobilization decreased PS throughout the 4 days of the stress sessions. Thus, the data suggest that different stress modalities result in distinct sleep responses, with immobilization producing the most dramatic alterations.

Cholinergic mechanisms in cocaine-induced genital reflexes in paradoxical sleep-deprived male rats.

In view of the fact that paradoxical sleep deprivation (PSD) modifies cocaine-induced genital reflexes (penile erection [PE] and ejaculation [EJ]), the aim of this study was to address the interaction of cholinergic agents with the action of cocaine on the genital reflexes of PSD male rats. After a 4-day period of PSD, each group was administered with cholinergic drugs 1 h prior to cocaine and was placed in observation cages. The administration of nicotine (0.12, 0.25, 0.5 and 1 mg/kg sc) reduced the frequency and number of animals displaying PE and increased PE latency. Pretreatment with mecamylamine (1.25, 5, 10 and 20 mg/kg sc) also significantly reduced PE frequency for all doses used. The percentage of rats showing EJ was significantly reduced in the group pretreated with 1 mg/kg of nicotine compared with the saline group. The administration of pilocarpine (1.25, 2.5, 5 and 10 mg/kg sc) and atropine (1.25, 5, 10 and 20 mg/kg sc) led to a reduction in the frequency of PE displayed by the rats. These data show that agonist and antagonist cholinergic drugs inhibit genital reflexes in PSD male rats injected with cocaine. The data also suggest that the stimulating action of cocaine in potentiating the sexual effects in PSD rats does not override the effects of the cholinergic mechanisms of sexual behavior.