Horm Metab Res 1995; 27(3): 121-125
DOI: 10.1055/s-2007-979922
Originals Basic

© Georg Thieme Verlag Stuttgart · New York

Reduced Prolactin Release during Immobilization Stress in Thyrotoxic Rats: Role of the Central Serotoninergic System

Maria José Ramalho1 , L. C. Reis2 , J. Antunes-Rodrigues3 , K. O. Nonaka4 , E. De Castro e Silva1
  • 1Departamento de Fisiologia, Instituto de Ciências da Saúde, Universidade Federal da Bahia, Salvador, Bahia
  • 2Departamento de Ciências Fisiológicas, Instituto de Biologia, Universidade Federal Rural do Rio de Janeiro, Itaguaí, Rio de Janeiro
  • 3Departamento de Fisiologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, São Paulo
  • 4Departamento de Ciências da Saúde, Centro de Ciências Biológicas e da Saúde, Universidade Federal de São Carlos, São Carlos, São Paulo, Brasil
Further Information

Publication History

1994

1994

Publication Date:
23 April 2007 (online)

Abstract

Adult Wistar male rats in a thyrotoxic state T4↑ rats) induced by administration of T4 (350 µg/kg/day, i.p. for 7 days) as well as their euthyroid controls were submitted to immobilization stress during forty minutes. Prolactin (PRL) secretion during stress was significantly lower in T4↑ rats as compared to control animals. Treatment with MK 212, a serotoninergic agonist, entirely reverts this situation. The effect of MK 212 seems to be due to its interaction with 5-HT2 receptors since it is blocked by LY 53857, a selective 5-HT2 antagonist. Furthermore, the blockade of 5-HT2 receptors by LY 53857, a selective 5-HT2 antagonist, significantly diminishes prolactin (PRL) response to stress in euthyroid rats but has no effect in T4↑ animals. It is suggested that an increased concentration of thyroid hormone in plasma disrupts an endogenous serotoninergic brain input necessary to trigger stress-induced PRL rise.

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