Abstract
Numerous experimental results, obtained in the last 10 years, have indicated that brain catecholaminergic systems are involved in the regulation of wakefulness and sleep. The investigation of the wakefulness mechanisms has given rather unambiguous results, pointing to a role of ascending neuronal systems containing norepinephrine (NE). Selective lesions of these systems by microinjection of 6-hydroxydopamine (6-OHDA), a drug inducing neurotoxic lesions of catecholamine (CA) neurons, result in a decrease of EEG waking, most pronounced during the first 4 days after the lesion, and followed by a gradual recovery11. Similarly, the administration of alpha-methylparatyrosine (αMPT), an inhibitor of CA synthesis through blockade of tyrosine hydroxylase, induces in animals a decrease of wakefulness, which can be temporarily reversed by microinjections of NE in the preoptic area or in the reticular activating systems19. These and other results indicate that an enhancement of activity in NE synapses induces EEG waking, whereas dopaminergic (DA) systems may be more specifically involved in behavioural wakefulness3.
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Gaillard, JM. (1979). Brain Catecholaminergic Activity in Relation to Sleep. In: Priest, R.G., Pletscher, A., Ward, J. (eds) Sleep Research. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-6226-5_4
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DOI: https://doi.org/10.1007/978-94-011-6226-5_4
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