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Richard S. Nishioka

Researcher at University of California, Berkeley

Publications -  108
Citations -  5447

Richard S. Nishioka is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Smoltification & Oreochromis mossambicus. The author has an hindex of 46, co-authored 108 publications receiving 5363 citations. Previous affiliations of Richard S. Nishioka include Washington State University & San Jose State University.

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Journal ArticleDOI

Urotensin II: a somatostatin-like peptide in the caudal neurosecretory system of fishes.

TL;DR: Urotensin II, a peptide hormone from the caudal neurosecretory system of the teleost, Gillichthys mirabilis, was isolated by using classical chromatographic techniques and high-performance liquid chromatography (HPLC) to establish its structure.
Book ChapterDOI

Neurohormones from fish tails: the caudal neurosecretory system. I. "Urophysiology" and the caudal neurosecretory system of fishes.

TL;DR: The caudal system in teleosts is heavily innervated, consistently by aminergic input and occasionally by cholinergic and peptidergic pathways from the brain this paper.
Journal ArticleDOI

Osmoregulatory Actions of Growth Hormone and Prolactin in an Advanced Teleost

TL;DR: Tilapia PRLs (PRL177 and PRL188) increased plasma osmolality in 100% seawater and reduced gill Na+,K(+)-ATPase activity, the effects induced byPRL188 being more significant than those by PRL177, indicating GH may be involved in seawater adaptation of tilapia, a species belonging to the most advanced teleost super-order.
Journal ArticleDOI

Control of prolactin secretion in teleosts, with special reference to Gillichthys mirabilis and Tilapia mossambica.

TL;DR: The results indicate that at least four mechanisms may be involved in the control of prolactin secretion in teleosts: inhibitory control from the hypothalamus presumably mediated by aminergic fibers, direct stimulation due to decreasing plasma osmotic pressure, negative feedback by either Prolactin itself or increased plasma sodium level, and stimulation by circulating estrogen.