The Octadecaneuropeptide Stimulates Somatolactin Release from Cultured Goldfish Pituitary Cells - Archive ouverte HAL Access content directly
Journal Articles Journal of Neuroendocrinology Year : 2013

The Octadecaneuropeptide Stimulates Somatolactin Release from Cultured Goldfish Pituitary Cells

Abstract

The present study aimed to investigate the distribution of the octadecaneuropeptide (ODN) in the goldfish brain and to look for a possible effect of ODN on somatolactin (SL) release from pituitary cells. A discrete population of ODN-immunoreactive neurones was localised in the lateral part of the nucleus lateralis tuberis. These neurones sent projections through the neurohypophyseal tract towards the neurohypophysis, and nerve fibres were seen in the close vicinity of SL-producing cells in the pars intermedia. Incubation of cultured goldfish pituitary cells with graded concentrations of ODN (10(-9) -10(-5 ) m) induced a dose-dependent stimulation of SL-β, but not SL-α, release. ODN-evoked SL release was blocked by the metabotrophic endozepine receptor antagonist cyclo(1-8) [DLeu(5) ]OP but was not affected by the central-type benzodiazepine receptor antagonist flumazenil. ODN-induced SL release was suppressed by treatment with the phospholipase C (PLC) inhibitor U-73122 but not with the protein kinase A (PKA) inhibitor H-89. These results indicate that, in fish, ODN produced by hypothalamic neurones acts as a hypophysiotrophic neuropeptide stimulating SL release. The effect of ODN is mediated through a metabotrophic endozepine receptor positively coupled to the PLC/inositol 1,4,5-trisphosphate/protein kinase C-signalling pathway.

Dates and versions

hal-01960648 , version 1 (19-12-2018)

Identifiers

Cite

A Azuma, K. Wada, Jérôme Leprince, M. Tonon, M. Uchiyama, et al.. The Octadecaneuropeptide Stimulates Somatolactin Release from Cultured Goldfish Pituitary Cells. Journal of Neuroendocrinology, 2013, 25 (3), pp.312-321. ⟨10.1111/jne.12005⟩. ⟨hal-01960648⟩
13 View
0 Download

Altmetric

Share

Gmail Facebook Twitter LinkedIn More