Thyroid hormone and estrogen regulate brain region-specific messenger ribonucleic acids encoding three gonadotropin-releasing hormone genes in sexually immature male fish, Oreochromis niloticus

Citation
Is. Parhar et al., Thyroid hormone and estrogen regulate brain region-specific messenger ribonucleic acids encoding three gonadotropin-releasing hormone genes in sexually immature male fish, Oreochromis niloticus, ENDOCRINOL, 141(5), 2000, pp. 1618-1626
Citations number
63
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINOLOGY
ISSN journal
00137227 → ACNP
Volume
141
Issue
5
Year of publication
2000
Pages
1618 - 1626
Database
ISI
SICI code
0013-7227(200005)141:5<1618:THAERB>2.0.ZU;2-K
Abstract
The present study was undertaken to determine whether T-3, estrogen, and 11 -ketotestosterone could alter a specific population of GnRH-containing neur ons, as indicated by a change in messenger RNA (mRNA) levels in sexually im mature male tilapia, Oreochromis niloticus. Two weeks after castration, fis h were assigned to four treatment groups. One group served as the control ( sesame oil); a single ip injection of (T-3; 5 mu g/g), estradiol benzoate ( EB; 5 mu g/g), Or 11-ketotestosterone (KT; 5 mu g/g) was administered to th e remaining three groups. Twenty-four hours after the injection, brains wer e collected and processed for in situ hybridization histochemistry using S- 35-labeled 30-mer antisense oligonucleotide probes complementary to the GnR H-coding region of chicken II, salmon, and seabream GnRH. Computerized imag e analysis was performed to quantify mRNA concentrations, neuronal numbers, and neuronal size of the terminal nerve-nucleus olfactoretinalis, preoptic , and midbrain GnRH neurons. KT had no effect on any of the above neuronal parameters examined for salmon or seabream GnRH. Neither T-3, EB, nor KT wa s effective to induce changes in midbrain chicken GnRH II mRNA concentratio ns, neuronal numbers, and neuronal size, indicating that an as yet unknown regulatory mechanism may operate midbrain GnRH neurons. T-3 specifically su ppressed the concentration of terminal nerve salmon GnRH mRNA, and EB signi ficantly increased preoptic seabream GnRH neuronal numbers. These results a re consistent with the hypothesis that thyroid hormone, by suppressing term inal nerve GnRH expression, promotes inhibition of sexual maturation. Furth ermore, the failure of KT, a nonaromatizable androgen, to influence preopti c GnRH neurons emphasizes that an estrogenic pathway, at the onset of sexua l maturation, is responsible for the recruitment of additional preoptic GnR H neurons that are fundamental to reproduction and behavior.