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The Octadecaneuropeptide Stimulates Somatolactin Release from Cultured Goldfish Pituitary Cells
Author(s) -
Azuma M.,
Wada K.,
Leprince J.,
To M.C.,
Uchiyama M.,
Takahashi A.,
Vaudry H.,
Matsuda K.
Publication year - 2013
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12005
Subject(s) - medicine , endocrinology , neuropeptide , biology , phospholipase c , protein kinase c , stimulation , receptor , antagonist , receptor antagonist , population , inositol phosphate , pars intermedia , inositol , pituitary gland , kinase , microbiology and biotechnology , hormone , environmental health
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 [ DL eu 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.