This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by DONOSO, A. O. Articles by McCANN, S. M. Search for Related Content PubMed PubMed Citation Articles by DONOSO, A. O. Articles by McCANN, S. M.

Effects of Drugs that Modify Brain Monoamine Concentrations on Plasma Gonadotropin and Prolactin Levels in the Rat

Department of Physiology, University of Texas Southwestern Medical School Dallas, Texas 75235

Abstract

DL--Methyltyrosine (-MT), which blocks catecholamine biosynthesis, produced a dramatic rise in plasma prolactin within 30 min of ip injection in castrated rats and treatment with -MT for 4 days resulted in continued high levels of plasma prolactin and an elevation of pituitary prolactin concentration and content. Plasma FSH and LH were not significantly altered by -MT. Selective blockade of norepinephrine (NE) biosynthesis with diethyldithiocarbamate (DDC) failed to alter prolactin levels but did lower plasma LH. Blockade of serotonin biosynthesis with p-chlorophenylalanine (p-CPA) failed to modify plasma levels of any of the 3 pituitary hormones measured and did not alter the elevation in plasma prolactin produced by concomitant administration of -MT. When L-dihydroxphenylalanine (L-DOPA) was administered to elevate brain catecholamines, it lowered plasma prolactin but failed to alter FSH and LH levels. This lowering of piolactin by L-DOPA still occurred if conversion of dopamine (DA) to NE was blocked by prior administration of DDC. In animals with elevated plasma prolactin as a result of -MT treatment, L-DOPA administration to bypass the block and normalize catecholamine biosynthesis produced a dramatic lowering of plasma prolactin which was not prevented by administering DDC. On the other hand, treatment of the -MT-treated rats with dihydroxyphenyl serine (DOPS) to normalize only NE synthesis resulted in a further elevation in prolactin levels. Treatment with pargyline to elevate levels of catecholamines and serotonin produced a lowering of plasma prolactin and LH but not FSH. In every case an expected alteration in brain DA was associated with the converse change in prolactin, providing strong support for the thesis that DA is an inhibitory transmitter which suppresses prolactin release. Elevated levels of NE may increase prolactin release and decreased NE may lower LH. (Endocrinology 89: 774, 1971)

Footnotes

¹ 1 Established Investigator, Consejo Nacional de Investigaciones Cientificas y Tecnicas de Argentina. Present address: Laboratorio de Investigaciones Cerebrales, Facultad de Ciencias Medicas, U.N. de Cuyo, Mendoza, Argentina. Preliminary reports of this work have been given at the Meeting of the Society for Biology (Chile) in September, 1970 and at the 53rd Meeting of the Endocrine Society, pg. 27, 1971.

² Postdoctoral Research Fellow from Facultad de Medicina, Departamento de Fisiopatologia, Universidad de los Andes, Merida, Venezuela.

³ Supported by USPHS Grant AM 10073 and by grants from the Ford Foundation and Texas Population Crisis Foundation.

Received December 9, 1970.

This article has been cited by other articles:

				E. J. Sachar, P. H. Gruen, T. B. Karasu, N. Altman, and A. G. Frantz Thioridazine Stimulates Prolactin Secretion in Man Arch Gen Psychiatry, July 1, 1975; 32(7): 885 - 886. [Abstract] [PDF]

				H. Y. Meltzer, E. J. Sachar, and A. G. Frantz Serum Prolactin Levels in Unmedicated Schizophrenic Patients Arch Gen Psychiatry, October 1, 1974; 31(4): 564 - 569. [Abstract] [PDF]