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  Noradrenaline inhibits exocytosis via the G protein βγ subunit and refilling of the readily releasable granule pool via the αi1/2 subunit.

Zhao, Y., Fang, Q., Straub, S. G., Lindau, M., & Sharp, G. W. G. (2010). Noradrenaline inhibits exocytosis via the G protein βγ subunit and refilling of the readily releasable granule pool via the αi1/2 subunit. Journal of Physiology, 588(18), 3485-3498. doi:10.1113/jphysiol.2010.190090.

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Zhao, Y., Author
Fang, Q., Author
Straub, S. G., Author
Lindau, M.1, Author              
Sharp, G. W. G., Author
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1Research Group of Nanoscale Cell Biology, MPI for Biophysical Chemistry, Max Planck Society, ou_1832294              

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 Abstract: The molecular mechanisms responsible for the ‘distal’ effect by which noradrenaline (NA) blocks exocytosis in the β-cell were examined by whole-cell and cell-attached patch clamp capacitance measurements in INS 832/13 β-cells. NA inhibited Ca2+-evoked exocytosis by reducing the number of exocytotic events, without modifying vesicle size. Fusion pore properties also were unaffected. NA-induced inhibition of exocytosis was abolished by a high level of Ca2+ influx, by intracellular application of antibodies against the G protein subunit Gβ and was mimicked by the myristoylated βγ-binding/activating peptide mSIRK. NA-induced inhibition was also abolished by treatment with BoNT/A, which cleaves the C-terminal nine amino acids of SNAP-25, and also by a SNAP-25 C-terminal-blocking peptide containing the BoNT/A cleavage site. These data indicate that inhibition of exocytosis by NA is downstream of increased [Ca2+]i and is mediated by an interaction between Gβγ and the C-terminus of SNAP-25, as is the case for inhibition of neurotransmitter release. Remarkably, in the course of this work, a novel effect of NA was discovered. NA induced a marked retardation of the rate of refilling of the readily releasable pool (RRP) of secretory granules. This retardation was specifically abolished by a Gαi1/2 blocking peptide demonstrating that the effect is mediated via activation of Gαi1 and/or Gαi2.

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Language(s): eng - English
 Dates: 2010-09-162010
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: DOI: 10.1113/jphysiol.2010.190090
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Title: Journal of Physiology
Source Genre: Journal
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Pages: - Volume / Issue: 588 (18) Sequence Number: - Start / End Page: 3485 - 3498 Identifier: -