Adrenergic and dopaminergic regulation of gonadotropin-releasing hormone release from goldfish preoptic-anterior hypothalamus and pituitary in vitro

Abstract

The involvement of adrenergic and dopaminergic receptor subtypes on in vitro release of radioimmunoassayable gonadotropin-releasing hormone (GnRH) from incubated preoptic-anterior hypothalamic (P-AH) slices and pituitary fragments of sexually mature male goldfish was studied. Norepinephrine (NE) produced a dose-related stimulation of GnRH from P-AH slices, but not from pituitary fragments. The effects of some adrenergic receptor agonists (1 μ M) on GnRH release from P-AH slices were tested: phenylephrine (α 1-agonist) significantly stimulated GnRH release; clonidine (α 2-agonist) and isoproterenol (β-agonist) were ineffective. Incubation of P-AH slices with phentolamine ( α 1 α 2 -antagonist ) and prazosin (α 1-antagonist), at a concentration of 1 μ M, inhibited the release of GnRH induced by NE (60 μ M); the α 2-antagonist yombibin and the β-antagonist propanolol were ineffective. None of the adrenergic antagonists (1 μ M) tested produced significant effects on spontaneous release of GnRH from both tissue preparations. Spontaneous release of GnRH from both P-AH slices and pituitary fragments was reduced by dopamine (DA) in a dose-related manner. The effects of some DA agonists (1 μ M) were tested: apomorphine ( D 1 D 2 -agonist ) and SKF 38398 (D 1-agonist), but not bromocriptine and LY-171555 (D 2-agonists) significantly reduced spontaneous GnRH release from P-AH slices in vitro. On the other hand, D 2-agonists, but not D 1-agonists, significantly reduced GnRH release from pituitary fragments. The effects of DA antagonists (1 μ M) were also tested: in P-AH slices, addition of SKF-83566 (D 1-antagonist) significantly reduced spontaneous GnRH release; pimozide and domperidone (D 2-antagonist) were ineffective when tested alone. However, none of the DA-antagonists blocked the DA-induced inhibition of GnRH release from P-AH slices. No significant effect was obtained on spontaneous GnRH release from pituitary fragments with any of the DA-antagonists when tested alone. Pimozide and domperidone reversed the DA-induced inhibition of GnRH release from pituitary fragments; SKF-83566 was ineffective. In conclusion, results in this study indicate that NE acts through α 1-adrenergic receptor to stimulate GnRH release from P-AH slices of sexually mature male goldfish in vitro. On the other hand, the inhibitory actions of DA on GnRH release from the P-AH region and pituitary involve pharmacologically distinct DA D 1- and D 2-receptors, respectively.