Evidence that it is possible to cause anorexia by increasing release and/or directly stimulating postsynaptic serotonin receptors in the brain

Rosario Samanin, Tiziana Mennini, Silvio Garattini

Research output: Contribution to journalArticlepeer-review

Abstract

1. 1. Recent pharmacological and biochemical data on the role of brain serotonin in the anorectic activity of some drugs are discussed. 2. 2. Quipazine and meta-chlorophenylpiperazine, two displacers of serotonin binding to brain membranes, caused powerful anorexia in rats. This effect was prevented by methergoline, a central serotonin antagonist, but not by various procedures known to interfere with brain catecholamines. 3. 3. LM 5008, a potent and specific inhibitor of serotonin neuronal uptake, did not significantly change food intake. Since, unlike fenfluramine, this compound does not markedly increase serotonin release nor does it act as an agonist at postsynaptic receptors, as quipazine and metachlorophenylpiperazine do, it is suggested that increased serotonin release and/or direct stimulation of postsynaptic receptors play a more important role than upake inhibition in the anorexia induced by drugs acting on brain serotonin.

Original languageEnglish
Pages (from-to)363-369
Number of pages7
JournalProgress in Neuro-Psychopharmacology
Volume4
Issue number4-5
DOIs
Publication statusPublished - 1980

Keywords

  • anorectic drugs
  • food intake
  • serotonin receptors
  • serotonin release
  • serotonin uptake

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Psychiatry and Mental health
  • Neuroscience(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Medicine(all)

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