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The effects of the dopamine (DA) receptor agonists apomorphine, bromocriptine and pergolide were compared with those produced by a DA receptor antagonist, haloperidol, in rats implanted with electrodes for chronic sleep recordings. Apomorphine (0.025-2.0 mg/kg) and bromocriptine (0.25-6.0 mg/kg) induced biphasic effects such that low doses decreased wakefulness (W) and increased slow wave sleep (SWS) and REM sleep (REMS), while large doses induced opposite effects. The effects of pergolide (0.05-0.5 mg/kg) on W and SWS were also biphasic, while REMS was suppressed over the range of dosages given. At 0.040 mg/kg, haloperidol increased W, while at 0.160 mg/kg it produced the opposite effect. Pretreatment with haloperidol (0.020 mg/kg) in a dose which preferentially acts at presynaptic sites reversed the effects of low doses of apomorphine, bromocriptine or pergolide on sleep and W. However, the compound differed substantially in its ability to block agonist effects. The increase in sleep after low doses of apomorphine, bromocriptine or pergolide could be related to activation of presynaptic D-2 receptors located on DA axons of mesolimbic and mesocortical systems. In addition, inhibition of norepinephrine and acetylcholine neurons having inhibitory D-2 receptors could contribute to the increase of sleep after small doses of the DA agonists.

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The H1-receptor agonist 2-thiazolylethylamine (2-TEA) given by i.c.v. route dose-dependently increased wakefulness (W) and decreased NREM sleep (NREMS) and REM sleep (REMS) in rats prepared for chronic sleep recordings. The H1-receptor antagonists pyrilamine and diphenhydramine given by i.p. route decreased W and increased NREMS. Pyrilamine prevented the increase of W and decrease of NREMS produced by 2-TEA. However, REMS reduction was not antagonized, what tends to suggest that two different mechanisms could be involved in the 2-TEA-induced effects on NREMS and REMS. Cimetidine which blocks H2-receptors, when given by i.p. route showed no significant effects on sleep and W. Administration of the H2-receptor agonist dimaprit and the H2-receptor antagonists cimetidine, metiamide and ranitidine by i.c.v. route induced the appearance of high voltage spikes at cortical leads, thus leaving inconclusive the matter of their effects on sleep and wakefulness. Our results tend to support the proposal that the H1-receptor intervenes in sleep-wakefulness regulation. Limitations in the available H2-receptor agonists and antagonists presently preclude a more detailed analysis of the role of H2-receptors on sleep and W.

No abstract