Catecholamines and the sleep-wake cycle I. EEG and behavioral arousal

摘要: Abstract The exact role of catecholamines (CA) on the sleep-wake cycle is still controversial. Critical analysis lesion studies tends to suggest a neuromodulatory for both dopamine (DA) and norepinephrine (NE) EEG behavioral arousal. Support this view provided by pharmacological in which catecholaminergic systems are activated or inhibited. Taken together they show that disturbances dynamic balance between neurochemical may alter conditions wake-triggering mechanisms express at optimal levels. Large electrolytic neurotoxic lesions affect noradrenergic dopaminergic structures associated with marked prolonged changes decreased arousal, respectively. In contrast, specific circumscribed damage restricted these followed transient decrease waking activity. Thus, results observed after large central most probably related destruction non-catecholaminergic neurons. Inhibition brain CA synthesis causes sedation Selective stimulation presynaptic alpha-adrenergic (∝ 2) receptors waking, while opposite effects result from ∝2-receptor blockade. Drugs agonistic activity postsynaptic (∝1) sites increase desynchronization, but blockade ∝1-receptor does not decreases EEG. treatments simultaneously block NE DA significantly waking. Beta-adrenergic receptor blockers no conclusive sleep. DA-receptor agonists induce biphasic effects, low doses decreasing increasing cortical desynchronization motility. Opposite laboratory animals injection blockers.