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      Effect of Serotonin 5-HT 1, 5-HT 2, and 5-HT 3 Receptor Antagonists on the Prolactin Response to Restraint and Ether Stress

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          Serotonin (5-HT) appears to be involved in the central control of the prolactin (PRL) response to suckling and estrogen. Furthermore, 5-HT may participate in the mediation of stress-induced PRL release. In order further to elucidate the role of 5-HT and the type of 5-HT receptor(s) involved in the PRL response to stress, we investigated the effect of blockade of 5-HT<sub>1</sub>, 5-HT<sub>2</sub> or 5-HT<sub>3</sub> receptors on the restraint or ether stress-induced release of PRL in male rats. Pretreatment with the 5-HT<sub>1 + 2</sub> receptor antagonist methysergide (0.5 or 2.5 mg/kg i.p.) inhibited or prevented the PRL response to restraint or ether stress. Pretreatment with the 5-HT<sub>2</sub> receptor antagonists ketanserin or LY 53857 (0.5 or 2.5 mg/kg i.p.) inhibited the response to restraint or ether stress approximately 30 or 60%, respectively. Higher doses of both 5-HT<sub>2</sub> receptor antagonists (10 mg/kg i.p.) had a minor inhibitory effect (5-30% for ketanserin and 50% for LY 53857). Prior intraperitoneal administration of the 5-HT<sub>3</sub> receptor antagonists ICS 205-930 or GR 38032F (0.05-2.5 mg/kg i.p.) inhibited the restraint stress-induced PRL release dose-dependently. Both compounds inhibited the PRL response to ether stress, but only the effect of GR was dose-related. The maximal inhibitory effect (70% inhibition of the PRL response to restraint or ether stress) was obtained for both compounds at a dose of 0.1 mg/kg. We conclude that serotonergic neurons are involved in the mediation of the stress-induced PRL release by activation of 5-HT<sub>1</sub>, 5-HT<sub>2</sub> as well as 5-HT<sub>3</sub> receptors.

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          Author and article information

          S. Karger AG
          07 April 2008
          : 56
          : 3
          : 371-377
          Department of Medical Physiology C, The Panum Institute, University of Copenhagen, Denmark
          126251 Neuroendocrinology 1992;56:371–377
          © 1992 S. Karger AG, Basel

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          Pages: 7
          Original Paper


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