title: Possible sites of dopaminergic inhibition of gonadotropin release from the pituitary of a teleost fish, tilapia.
abstract: The present study is an attempt to find sites of dopaminergic inhibition along the transduction cascades culminating in gonadotropin (GtH) release in a teleost fish, tilapia. Experiments were carried out on perifused pituitary fragments and in primary culture of trypsinized pituitary cells. Salmon GnRH, chicken GnRH I and II stimulated GtH release in culture with estimated ED50 values of 15.56 pM, 2.55 nM and 8.65 pM, respectively. Apomorphine (APO; 1 microM) totally abolished this stimulation. Dopamine (DA; 1 microM) reduced both basal and GnRHa-stimulated GtH release from perifused pituitary fragments but did not alter the formation of cAMP. In a similar perifusion experiment DA abolished GtH release in response to forskolin (10 microM) with no reduction in cAMP formation. This indicates that one site of the dopaminergic inhibition is distal to cAMP formation, an indication not compatible with the classic characteristic of DA D2 type mode of action. The inhibition of GtH release in culture, caused by 1 microM APO, the specific DA D2 agonists LY 171555 (LY) or bromocryptine (BRCR) could not be reversed by activating protein kinase C (PKC) by DiC8 or the phorbol ester TPA. This would indicate a site for DA action distal to PKC. However, the stimulatory effect of arachidonic acid (AA; 50 microM) in perifusion was not reduced by DA (1 microM) or by APO, LY or BRCR in culture, which suggests a site for DA action proximal to AA formation. APO, LY and BRCR reduced GtH release in response to the Ca2+ ionophore A23187, however, their inhibitory effect was reversed by 10 microM ionomycin.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Zoology, Tel-Aviv University, Israel.
authors.forename: B
authors.initials: B
authors.lastname: Levavi-Sivan
authors.forename: M
authors.initials: M
authors.lastname: Ofir
authors.forename: Z
authors.initials: Z
authors.lastname: Yaron
mesh_terms: D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D016718:Arachidonic Acid / Q000378:metabolism; D001971:Bromocriptine / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000096:biosynthesis; D004075:Diglycerides / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology / Q000502:physiology*; D018491:Dopamine Agonists / Q000494:pharmacology; D004873:Ergolines / Q000494:pharmacology; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D006065:Gonadotropins, Pituitary / Q000378:metabolism*; D015759:Ionomycin / Q000494:pharmacology; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism*; D019257:Quinpirole; D015398:Signal Transduction; D017210:Tilapia / Q000502:physiology*
chemical_list: D004075:Diglycerides; D018491:Dopamine Agonists; D004873:Ergolines; D006065:Gonadotropins, Pituitary; C044295:1,2-dioctanoylglycerol; D005576:Colforsin; D019257:Quinpirole; D016718:Arachidonic Acid; D007987:Gonadotropin-Releasing Hormone; D000001:Calcimycin; D001971:Bromocriptine; D015759:Ionomycin; D000242:Cyclic AMP; D001058:Apomorphine; D002118:Calcium; D004298:Dopamine