Salsolinol, an antagonist of prolactoliberine, induces an increase in plasma catecholamine levels in the rat

Boris Mravec, Ibolya Bodnar, Marton I.K. Fekete, Gyorgy M. Nagy, Richard Kvetnansky

Research output: Contribution to journalArticle

14 Citations (Scopus)


It has been recently observed that salsolinol (1-methyl-6,7-dihydroxy-1,2, 3,4-tetrahydroisoquinoline), a putative endogenous prolactin-releasing factor is a potent inhibitor of stress-induced release of epinephrine and norepinephrine. The prolactin release caused by salsolinol was inhibited by 1-methyl-3,4-dihydroisoquinoline (1MeDIQ). Therefore, the aim of our present studies was to investigate the effect of 1MeDIQ on plasma catecholamine levels. It has been found that 1MeDIQ is able to induce a massive increase in plasma catecholamine levels. Pretreatment of the animals with a ganglionic blocker, chlorisondamine, could completely abolish the effect of 1MeDIQ on plasma norepinephrine, and plasma epinephrine levels were only significantly attenuated. Spinal cord transection between cervical and thoracic segments eliminated 1MeDIQ induced increase in epinephrine, whereas increase in plasma norepinephrine was not affected. Hence, this effect of 1MeDIQ on sympathoadrenal system activity is most probably mediated through the level of sympathetic ganglia or partially at more centrally located sites of the nervous system. These results suggest that elevation of plasma catecholamines is involved in the mechanism of action of 1MeDIQ inhibiting the biological effect of salsolinol.

Original languageEnglish
Pages (from-to)35-40
Number of pages6
JournalAutonomic Neuroscience: Basic and Clinical
Issue number1-2
Publication statusPublished - Sep 30 2004


  • 1MeDIQ
  • Chlorisondamine
  • Epinephrine
  • Norepinephrine
  • Plasma catecholamines
  • Prolactoliberine-salsolinol
  • Spinal cord transection

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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