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Lipid secretory mechanisms in the mammalian Harderian gland
Author(s) -
Satoh Yohichi,
Gesase Ainory Peter,
Habara Yoshiaki,
Ono Kazuyuki,
Kanno Tomio
Publication year - 1996
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/(sici)1097-0029(19960601)34:2<104::aid-jemt2>3.0.co;2-s
Subject(s) - harderian gland , biology , microbiology and biotechnology , lipid signaling , secretory iga , secretion , lipid metabolism , endocrinology , chemistry , biochemistry , immunology , receptor , antibody
The mammalian Harderian glands are lipid‐secreting glands. In an unstimulated condition, the glandular cells frequently exocytose the lipid materials; however, no intracellular calcium ion ([Ca 2+ ] c ) changes are detectable. Cholinergic (muscarinic) secretagogues induce secretory activity and increase of [Ca 2+ ] c . A G‐protein activator, sodium fluoride, enhances the secretory activity and increase of [Ca 2+ ] c . Removal of extracellular calcium ions inhibits the secretion enhanced by cholinergic stimulation. Under pharmacologic stimulation, glandular cells may show an apocrine‐like secretory pattern. Cholinergic stimulation also induces contraction of the myoepithelial cells covering glandular end pieces; however, the reduction in volume of glandular end pieces is not prominent. Catecholamines have no effect on the release of lipid materials. These results indicate the involvement of G‐proteins linking with muscarinic receptors and Ca 2+ dynamics (increase of [Ca 2+ ] c and Ca 2+ influx) in lipid secretion by glandular cells and in contraction of myoepithelial cells of mammalian Harderian glands. However, the increase of [Ca 2+ ] c in Harderian glands was less when compared with other cells—for instance, those which secrete protein. © 1996 Wiley‐Liss, Inc.