Effects of galanin-monoaminergic interactions on vasopressin secretion in rat neurohypophyseal cell cultures

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The effects of dopamine (DA), serotonin (5-HT), histamine (HA), adrenaline (ADR), noradrenaline (NADR) and K+ administration on vasopressin (VP) secretion were studied in 13-14-day cultures of rat neurohypophyseal (NH) cells, and it was examined whether galanin (GAL) can modify the VP release enhancement induced by these monoaminergic compounds. An enzymatic dissociation technique was used to make the rat NH cell cultures. The VP contents of the supernatants of 14-day cultures were determined by radioimmunoassay. Following the administration of 10- 6 M GAL, the VP secretion into the supernatant media decreased. DA, 5-HT, ADR or NADR treatment increased the VP level substantially, while the enhancing effect of HA was more moderate. GAL administration before DA, ADR and NADR treatment prevented the VP concentration increase induced by DA, ADR or NADR. Preincubation with GAL reduced the 5-HT- or HA-induced VP level increases; the VP concentrations of the supernatant media remained above the control level. The GAL blocking effect was prevented by previous treatment with the GAL receptor antagonist galantid (M15). GAL had no effect on the VP level increase induced by K+, which causes a non-specific hormone secretion. The results indicate that the changes in VP secretion induced by the monoaminergic system can be directly influenced by the GAL-ergic system. The interactions between the monoaminergic and GAL-ergic systems regarding VP secretion occur at the level of the posterior pituitary.

Original languageEnglish
Pages (from-to)76-80
Number of pages5
JournalRegulatory Peptides
Issue number1-3
Publication statusPublished - Jun 5 2009



  • Adrenaline
  • Dopamine
  • Galanin
  • Histamine
  • Neurohypophyseal cell culture
  • Noradrenaline
  • Serotonin
  • Vasopressin

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

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