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Publisher Summary This chapter elaborates the NE-neurons and phasic sleep phenomena. Stimulation of adrenergic receptors by small doses of Clonidine i.v. decreased the PGO-waves in a dose-dependent way, and they were virtually abolished after 0–3 mg/kg. High doses of NE injected into a lateral ventricle have the same effect. DA by the same route has less than 1/10 the potency of NE. Dexamphetamine almost abolished PGO-waves. Inhibitors of the reuptake of NE, desipramine reduced the density of PGO-waves probably by increasing the concentration of NE in synapses. These drugs were, however, less potent than the tertiary tricyclic amines known to inhibit also the uptake of serotonin. Most agents studied have multiple effects on the CNS and alter the degree of alertness. It seems unlikely that the PGO waves depend exclusively upon the activity of monoamine neuron systems. No single isolated observation reported above can be accepted as evidence in favor of the role of NE in PGO-wave regulation. It is found that when all findings are taken together, the conclusion appears inevitable that a NE neuron system exerts a tonic inhibitory influence on PGO-waves. |
