Chronic beta-adrenergic stimulation increases in mice the sensitivity to methysergide and the number of cerebral high affinity serotonin binding sites (5-HT-1)

J Neural Transm. 1986;67(3-4):215-24. doi: 10.1007/BF01243349.

Abstract

Reserpine administration in mice causes, among other effects an akinesia which can be reversed by the serotonin agonist-antagonist methysergide. The effect of methysergide is potentiated by clenbuterol, a beta-adrenergic agonist, which itself causes hypomotility. Potentiation is weak after a single injection of clenbuterol, but becomes much stronger after repeated administration for 12 days. This treatment also causes a 50% increase in the number of high affinity 5-HT-1 binding sites in the brain. This increase would explain the increased potency of methysergide against reserpine-induced akinesia. These results show that: a beta-adrenergic drug, clenbuterol modulates the serotoninergic system; this modulation takes its importance after chronic treatment only; this interrelation may be important in depressive illness since it is observed on a test used in the screening of antidepressant drugs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Binding Sites / drug effects
  • Brain / drug effects*
  • Brain / metabolism
  • Clenbuterol / administration & dosage*
  • Drug Synergism
  • Ethanolamines / administration & dosage*
  • Male
  • Methysergide / administration & dosage*
  • Mice
  • Movement Disorders / chemically induced
  • Receptors, Adrenergic, beta / drug effects*
  • Reserpine / antagonists & inhibitors
  • Serotonin / metabolism*

Substances

  • Ethanolamines
  • Receptors, Adrenergic, beta
  • Serotonin
  • Reserpine
  • Clenbuterol
  • Methysergide