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The role of β- and α-adrenoceptors in the regulation of the stages of the sleep-waking cycle in the cat

Authors
Journal
Brain Research
0006-8993
Publisher
Elsevier
Publication Date
Volume
277
Issue
1
Identifiers
DOI: 10.1016/0006-8993(83)90912-5
Keywords
  • β-Adrenoceptors
  • α-Adrenoceptors
  • Sleep Stages
  • Prenalterol
  • Salbutamol
  • Atenolol
  • Metoprolol
  • Propranolol
  • Clonidine
  • Prazosin
  • Phentolamine

Abstract

Abstract The effects of β-adrenergic drugs alone and in combination with α-adrenergic drugs on the stages of the sleep-waking cycle were studied in adult cats. Polygraphic sleep recordings of 16 h showed that prenalterol (20 and 40 mg/kg i.p.), a β 1-adrenoceptor-stimulating drug increased paradoxical sleep (PS) in a dose-related manner during 4–12 h. Salbutamol (40 mg/kg), a β 2-adrenoceptor-stimulating drug, decreased PS during the first 4 h. Metoprolol (10 and 50 mg/kg), a relatively selective β 1-adrenoceptor blocking drug, increased drowsy waking during the first 4 h. The larger dose also tended to decrease PS. Already at the lower dose metoprolol partially antagonized the PS increase produced by prazosin, an α 1-adrenoceptor blocking drug. Propranolol (5 mg/kg), a β 1-andβ 2-adrenoceptor blocking drug, which alone decreases PS, antagonized the PS increase induced by phentolamine, an α 1-andα 2-adrenoceptor drug. Atenolol (5 mg/kg), a poorly lipid-soluble β-adrenoceptor blocking drug, failed to counteract phentolamine in increasing PS. Metoprolol (10 and 50 mg/kg) and propranolol (5 mg/kg) clearly potentiated the increase in drowsy waking and decrease in deep slow wave sleep and PS induced by clonidine (0.01 mg/kg), an α 2-adrenoceptor-stimulating drug. The results support the involvement of β-adrenoceptors in the regulation of the sleep-waking cycle. A high level of β-adrenergic activity may facilitate the production of PS. A low level of β-adrenergic activity, especially in combination with a high level of α 2-adrenergic activity, may facilitate the production of drowsy waking. Central α 1-andβ 1-adrenoceptors may mediate opposite functions in the regulation of PS.

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