Central and peripheral localization of somatostatin. Immunoenzyme immunocytochemical studies.
Author(s) -
J. A. Parsons,
Stanley L. Erlandsen,
Orion D Hegre,
Robert C. McEvoy,
Robert Elde
Publication year - 1976
Publication title -
journal of histochemistry and cytochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.971
H-Index - 124
eISSN - 1551-5044
pISSN - 0022-1554
DOI - 10.1177/24.7.60436
Subject(s) - somatostatin , immunocytochemistry , peripheral , chemistry , biology , medicine , endocrinology
Early in 1973, Brazeau et al. (5), using monolayer cultures of rat pituitary as a bioassay system (34), reported their findings on the chemical structure and physiology of a tetradecapeptide extracted from sheep hypothalami. The new neunohonmone was named somatostatin (SRIF) because it blocked the secretion of growth hormone. Synthetic SRIF proved to be an effective hapten in conjunction with immunogenic molecules, and anti-SRIF antisera were raised in rabbits (3, 7) and guinea pigs (10). Thus, very soon after the initial description of SRIF (5), specific antibodies became available for use in quantitative immunochemical and morphologic cytoendoncninologic studies. Accordingly, Animura et al. (2) and Patel et al. (23) synthesized a tyrosine-containing analogue of SRIF that could be readily iodinated and developed radioimmunoassays (RIA). Subsequent RIA of extracts of brains and peripheral tissues of experimental animals showed that SRIF was not localized exclusively within the hypothalamus. Immunoassayable SRIF is present in significant amounts within extnahypothalamic neural tissue (6, 23, 28) and also within tissues of the gastroentenopancreatic (GEP; see Fujita and Kobayashi (13)) system of endocrine cells (3, 28). Thus SRIF may play a physiologically significant role in these tissues as well as in the hypothalamus. This prospect has become more intriguing in light of numerous reports which have demonstrated that synthetic SRIF, in addition to its inhibitory actions upon adenohypophysial function, blocks pancreatic insulin and glucagon release (see Genich et aL (14), Reichlin et at. (28) and Vale et at. (33)).
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