RESUMEN
In Atlantic salmon (Salmo salar), seasonal photoperiod is shown to regulate the onset of sexual maturation, yet which brain region(s) is involved, and how light information impacts the neuroendocrine system are still not fully understood in teleosts. Detailed knowledge about the photoperiodic regulation of maturation in fish is still missing. In birds, it is shown that gonadotropin-releasing hormone (Gnrh) is located in the same neurons as vertebrate ancient (VA) opsin, suggesting a direct photoreceptive regulation for the onset of sexual maturity. This study presents a comprehensive topographic mapping of gnrh2, gnrh3, kisspeptin 2 (kiss2), gonadotropin-inhibiting hormone (gnih), and VA opsin using in situ hybridization on mature Atlantic salmon brains. Neurons positive for gnrh3 are expressed in the olfactory bulb and ventral telencephalon, while gnrh2-positive neurons are located dorsally in the midbrain tegmentum. Gonadotropin-inhibiting hormone (Gnih)-expressing cell bodies are present in the ventral thalamus and extend caudally to the hypothalamus with kiss2-expressing cells appearing in a lateral position. VA opsin-positive cells are present in the telencephalon, the rostro-dorsal ring of the left habenula, the ventral thalamus, and the midbrain tegmentum. The results show no similar co-location as found in birds, hypothesizing that the photoreceptive modulation of Gnrh in salmon may interact through neuronal networks. The topography analyses of the essential neuroendocrine cells related to sexual maturation in the Atlantic salmon brain show that diencephalic (thalamus, hypothalamus) and midbrain (tegmentum) regions seem central for controlling sexual maturation.
Asunto(s)
Células Neuroendocrinas , Salmo salar , Animales , Opsinas/metabolismo , Salmo salar/metabolismo , Células Neuroendocrinas/metabolismo , Maduración Sexual , Hormona Liberadora de Gonadotropina/metabolismo , Encéfalo/metabolismo , Gonadotropinas/metabolismoRESUMEN
We recently characterized two paralogs of the thyrotropin (TSH) beta subunit in Atlantic salmon, tshßa and tshßb, issued from teleost-specific whole genome duplication. The transcript expression of tshßb, but not of tshßa, peaks at the time of smoltification, which revealed a specific involvement of tshßb paralog in this metamorphic event. Tshßa and tshßb are expressed by distinct pituitary cells in salmon, likely related to TSH cells from the pars distalis and pars tuberalis, respectively, in mammals and birds. The present study aimed at investigating the neuroendocrine and endocrine factors potentially involved in the differential regulation of tshßa and tshßb paralogs, using primary cultures of Atlantic salmon pituitary cells. The effects of various neurohormones and endocrine factors potentially involved in the control of development, growth, and metabolism were tested. Transcript levels of tshßa and tshßb were measured by qPCR, as well as those of growth hormone (gh), for comparison and validation. Corticotropin-releasing hormone (CRH) stimulated tshßa transcript levels in agreement with its potential role in the thyrotropic axis in teleosts, but had no effect on tshßb paralog, while it also stimulated gh transcript levels. Thyrotropin-releasing hormone (TRH) had no effect on neither tshß paralogs nor gh. Somatostatin (SRIH) had no effects on both tshß paralogs, while it exerted a canonical inhibitory effect on gh transcript levels. Thyroid hormones [triiodothyronine (T3) and thyroxine (T4)] inhibited transcript levels of both tshß paralogs, as well as gh, but with a much stronger effect on tshßa than on tshßb and gh. Conversely, cortisol had a stronger inhibitory effect on tshßb than tshßa, while no effect on gh. Remarkably, insulin-like growth factor 1 (IGF1) dose-dependently stimulated tshßb transcript levels, while it had no effect on tshßa, and a classical inhibitory effect on gh. This study provides the first data on the neuroendocrine factors involved in the differential regulation of the expression of the two tshß paralogs. It suggests that IGF1 may be involved in triggering the expression peak of the tshßb paralog at smoltification, thus representing a potential internal signal in the link between body growth and smoltification metamorphosis.