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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1998-4-29
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pubmed:abstractText |
1. Endocytosis following exocytosis evoked by single step depolarizations was examined in bovine adrenal chromaffin cells using high resolution capacitance measurements in perforated-patch voltage clamp recordings. 2. Endocytosis was detected as a smooth exponential decline in membrane capacitance to either the pre-stimulus level ('compensatory retrieval') or far below the pre-stimulus level ('excess retrieval'). During excess retrieval, > 10% of the cell surface could be internalized in under 5 s. 3. Compensatory retrieval was equal in magnitude to stimulus-evoked exocytosis for membrane additions > 100 fF (about fifty large dense-cored vesicles). In contrast, excess retrieval surpassed both the stimulus-evoked exocytosis, and the initial capacitance level recorded at the onset of phase-tracking measurements. Cell capacitance was not maintained at the level achieved by excess retrieval but slowly returned to pre-stimulus levels, even in the absence of stimulation. 4. A large percentage of capacitance increases < 100 fF, usually evoked by 40 ms depolarizations, were not accompanied by membrane retrieval. 5. Compensatory retrieval could occur with any amount of Ca2+ entry, but excess retrieval was never triggered below a threshold Ca2+ current integral of 70 pC. 6. The kinetics of compensatory and excess retrieval differed by an order of magnitude. Compensatory retrieval was usually fitted with a single exponential function that had a median time constant of 5.7 s. Excess retrieval usually occurred with double exponential kinetics that had an extremely fast first time constant (median, 670 ms) and a second time constant indistinguishable from that of compensatory retrieval. 7. The speed of compensatory retrieval was Ca2+ dependent: the largest mono-exponential time constants occurred for the smallest amounts of Ca2+ entry and decreased with increasing Ca2+ entry. The Ca2+ dependence of mono-exponential time constants was disrupted by cyclosporin A (CsA), an inhibitor of the Ca(2+)- and calmodulin-dependent phosphatase calcineurin. 8. CsA also reduced the proportion of responses with excess retrieval, but this action was caused by a shift in Ca2+ entry values below the threshold for activation. The lower total Ca2+ entry in the presence of CsA was due to an increase in the rate of Ca2+ current inactivation rather than a reduction in peak amplitude. 9. Our data suggest that compensatory and excess retrieval represent two independent, Ca(2+)-regulated mechanisms of rapid membrane internalization in bovine adrenal chromaffin cells. Alternatively, there is a single membrane internalization mechanism that can switch between two distinct modes of behaviour.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-1374612,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-14731821,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-1538782,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-1645735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-1715244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-1961743,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-2172839,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-2223095,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-2459299,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-2546935,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-2611329,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-6330098,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-6607255,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-6959149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-7522234,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-7667289,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-7696493,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-7946334,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8052858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8065451,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8120090,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8145165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8412305,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8427700,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8529573,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8558477,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8562084,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8613758,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8735690,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8755485,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8778287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8785046,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8794084,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8799897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8814606,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8842011,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8893033,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9503324-8909551
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
506 ( Pt 3)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
591-608
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9503324-Adrenal Glands,
pubmed-meshheading:9503324-Animals,
pubmed-meshheading:9503324-Calcineurin,
pubmed-meshheading:9503324-Calcium,
pubmed-meshheading:9503324-Cattle,
pubmed-meshheading:9503324-Cell Membrane,
pubmed-meshheading:9503324-Cells, Cultured,
pubmed-meshheading:9503324-Chromaffin Cells,
pubmed-meshheading:9503324-Cyclosporine,
pubmed-meshheading:9503324-Electric Stimulation,
pubmed-meshheading:9503324-Electrophysiology,
pubmed-meshheading:9503324-Endocytosis,
pubmed-meshheading:9503324-Enzyme Inhibitors,
pubmed-meshheading:9503324-Kinetics,
pubmed-meshheading:9503324-Membrane Potentials,
pubmed-meshheading:9503324-Patch-Clamp Techniques
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pubmed:year |
1998
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pubmed:articleTitle |
Compensatory and excess retrieval: two types of endocytosis following single step depolarizations in bovine adrenal chromaffin cells.
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pubmed:affiliation |
Department of Neurobiology and Anatomy, Allegheny University of the Health Sciences, Medical College of Pennsylvania, Hahnemann University, Philadelphia, PA 19129, USA. ENGISCH@auhs.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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