Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/69285
標題: Voltage-dependent calcium channels in the corpora allata of the adult male loreyi leafworm, Mythimna loreyi
作者: Hsieh, Y.C.
Yang, E.C.
Hsu, E.L.
Chow, Y.S.
Kou, R.
關鍵字: juvenile hormone acids
cytosolic free Ca(2+) concentration
voltage-dependent calcium channel antagonists
juvenile-hormone biosynthesis
manduca-sexta
ca2+ channels
duponchel
lepidoptera
diploptera-punctata
release products
leucania-loreyi
corpus allatum
in-vitro
cells
期刊/報告no:: Insect Biochemistry and Molecular Biology, Volume 32, Issue 5, Page(s) 547-557.
摘要: In the corpora allata (CA) of the adult male loreyi leafworm, Mythimna loreyi, juvenile hormone acid (JHA) biosynthesis and release show a dose dependence on extracellular Ca(2+) concentration. Maxima are obtained with Ca(2+) concentrations of 2-10 mM, and synthesis and release are significantly inhibited under a Ca(2+)-free condition. The Ca(2+)-free inhibition of JHA release can be reversed by returning the glands to medium at 5 mM Ca(2+). The cytosolic free Ca(2+) concentration ([Ca(2+)](i)), which was measured with fura-2, in individual CA cells also shows a dose dependence on extracellular Ca(2+) concentration, with significant [Ca(2+)](i) depression being observed in the absence of extracellular Ca(2+). High K(+) significantly increases the JHA release and causes a transient [Ca(2+)](i) increase within seconds in CA cells. High-K(+)-stimulated JHA release is partially inhibited by the benzothiazepine (BTZ)-, dihydropyridine (DHP)- and phenylalkylamine (PAA)-sensitive L-type voltage-dependent calcium channel (VDCC) antagonists diltiazem, nifedipine and verapamil, respectively; by the N- and P/Q-type VDCC antagonist omega-conotoxin (omega-CgTx) MVIIC; and by the T-type VDCC antagonist amiloride. The N-type antagonist omega-CgTx GVIA is the most potent in inhibiting the high-K(+)-stimulated JHA release. No inhibitory effect is shown by the P-type antagonist omega-agatoxin TK (omega-Aga TK). The high-K(+)-induced transient [Ca(2+)](i) increase is largely inhibited by the L-type antagonists (diltiazem, nifedipine, verapamil), by the N- and P/Q-type antagonist omega-CgTx MVIIC and by the T-type antagonist amiloride, and is totally inhibited by the N-type antagonist omega-CgTx GVIA. No inhibitory effect is shown by the P-type antagonist omega-Aga TK. We hypothesize that L-type, N-type and T-type VDCCs may be involved to different degrees in the high-K(+)-stimulated JHA release and transient [Ca(2+)](i) increase in the individual CA cells of the adult male M. loreyi, and that the N-type VDCCs may play important roles in these cellular events. (C) 2002 Elsevier Science Ltd. All rights reserved.
URI: http://hdl.handle.net/11455/69285
ISSN: 0965-1748
文章連結: http://dx.doi.org/10.1016/s0965-1748(01)00133-3
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