Interactions of Catecholamines and GnRH in Regulation of Gonadotropin Secretion in Teleost Fish
| Autor: | R.E. Peter, M. Sokolowska, S. H. Shih, Billard R, Omeljaniuk Rj, C.S. Nahorniak, John P. Chang |
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| Rok vydání: | 1986 |
| Předmět: |
endocrine system
0303 health sciences medicine.medical_specialty medicine.drug_class Biology Inhibitory postsynaptic potential Gonadotropin secretion 03 medical and health sciences 0302 clinical medicine Endocrinology Dopamine Internal medicine medicine Catecholamine Fish Secretion Gonadotropin 030217 neurology & neurosurgery 030304 developmental biology medicine.drug Hormone |
| DOI: | 10.1016/b978-0-12-571142-5.50016-1 |
| Popis: | Publisher Summary This chapter highlights the interactions of catecholamine and gonadotropin-releasing hormone (GnRH) in regulation of gonadotropin secretion in teleost fish. It discusses that gonadotropin (GtH) release is under the stimulatory influence of GnRH and the inhibitory control of catecholamine dopamine (DA). DA acts as a GRIF to directly inhibit spontaneous GtH release and modulate GnRH action. The intensity of the DA inhibitory tone differs among the species and the intensity may also change along with the sexual recrudescence or maturation within the same species. In species such as the goldfish, the inhibitory DA influence is intense and the removal of this inhibitory tone is part of the mechanism regulating the ovulatory GtH increase. In the goldfish, although NE can directly stimulate GtH release, it may also act centrally to increase GtH secretion. The stimulatory influence of NE on GtH secretion is seasonal, dependent on the stage of gonadal recrudescence. Information on the possible participation of other neurotransmitters in the neuroendocrine regulation of GtH release in teleost is not available. Although it is generally believed that the neurotransmitters do not exert a direct influence on the pituitary to modify gonadotropin release in mammals, results from some studies on humans, rabbits, and ewes are strongly suggestive of a direct inhibitory DA influence on LH release. |
| Databáze: | OpenAIRE |
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