Effects of bromocriptine and α-flupenthixol on sleep in REM sleep deprived rats
Abstract
Administration of bromocriptine mesylate (5 mg/kg, i.p.), a dopamine receptor stimulant, to rats which were deprived of REM sleep for 24 hours resulted in a significant increase in wakefulness as well as significant reduction of REM sleep during the first 5 hours of EEG recording. These effects were completely abolished by pretreatment with α-flupenthixol (0.2 mg/kg, i.p.), a dopamine receptor blocker. The loss of REM sleep has not been regained during the next 25 hours of EEG recording suggesting that the stimulation of dopamine receptors reduced REM sleep without causing subsequent REM rebound. These data raise questions on the negative dopamine control of REM sleep and on the potential use of dopamine stimulants in clinical situations characterized by excessive REM or by REM sleep dysfunction (narcolepsy).
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Catecholamines and the sleep-wake cycle II. REM sleep
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Catecholamines and the sleep-wake cycle I. EEG and behavioral arousal
1982, Life SciencesThe exact role of catecholamines (CA) on the sleep-wake cycle is still controversial. Critical analysis of lesion studies tends to suggest a neuromodulatory role for both dopamine (DA) and norepinephrine (NE) on EEG and behavioral arousal. Support for this view is provided by pharmacological studies in which catecholaminergic systems are activated or inhibited. Taken together they show that disturbances in the dynamic balance between neurochemical systems may alter the conditions for wake-triggering mechanisms to express at optimal levels. Large electrolytic or neurotoxic lesions which affect noradrenergic and dopaminergic structures are associated with marked and prolonged EEG changes and decreased behavioral arousal, respectively. In contrast, specific and circumscribed damage restricted to these systems is followed by a transient decrease in waking activity. Thus, results observed after large central lesions are most probably related to destruction of non-catecholaminergic neurons. Inhibition of brain CA synthesis causes behavioral sedation and a decrease in waking activity. Selective pharmacological stimulation of presynaptic alpha-adrenergic (∝ 2) receptors tends to decrease waking, while opposite effects result from ∝2-receptor blockade. Drugs with agonistic activity at postsynaptic alpha-adrenergic (∝1) sites increase EEG desynchronization, but specific blockade of ∝1-receptor does not result in marked decreases of waking EEG. In contrast, treatments which simultaneously block NE and DA receptors significantly affect waking. Beta-adrenergic receptor blockers show no conclusive effects on waking or sleep. Selective DA-receptor agonists induce biphasic effects, with low doses decreasing and large doses increasing cortical desynchronization and motility. Opposite effects are observed in laboratory animals after injection of specific DA-receptor blockers.