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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
1995-5-11
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pubmed:abstractText |
The traditional function of neurotransmitter-gated ion channels is to induce rapid changes in electrical activity. Channels that are Ca(2+)-permeable, such as N-methyl-D-aspartate receptors at depolarized membrane potentials, can have a broader repertoire of consequences, including changes in synaptic efficacy, developmental plasticity, and excitotoxicity. Neuronal nicotinic receptors for acetylcholine (nAChRs) are usually less Ca(2+)-permeable than N-methyl-D-aspartate receptors but have a significant Ca2+ permeability, which is greater at negative potentials. Here we report that in neuroendocrine cells, activation of nAChRs can trigger exocytosis at hyperpolarized potentials. We used whole-cell patch-clamp recordings to record currents and the capacitance detection technique to monitor exocytosis in isolated bovine chromaffin cells. Stimulation of nAChRs at hyperpolarized potentials (-60 or -90 mV) evokes a large current and a maximal capacitance increase corresponding to the fusion of approximately 200 large dense-core vesicles. The amount of exocytosis is controlled both by the Ca2+ influx through nAChRs and by a contribution from thapsigargin-sensitive Ca2+ sequestering stores. This is a form of neurotransmitter action in which activation of nAChRs triggers secretion through an additional coupling pathway that coexists with classical voltage-dependent Ca2+ entry.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1018274,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1309647,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1309806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1370370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1432709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1463451,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1538782,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1645735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1675264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-16992152,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1700083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1726596,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1826518,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-1898353,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-2138778,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-2493078,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-2530452,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-2611329,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-2789101,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-3395658,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-6050606,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-6959149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-7520693,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8002966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8083751,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8254522,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8271224,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8369415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8391933,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8414901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7708776-8469610
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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 |
Mar
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
28
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pubmed:volume |
92
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3065-9
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:7708776-Adrenal Medulla,
pubmed-meshheading:7708776-Animals,
pubmed-meshheading:7708776-Calcium,
pubmed-meshheading:7708776-Calcium-Transporting ATPases,
pubmed-meshheading:7708776-Cattle,
pubmed-meshheading:7708776-Cells, Cultured,
pubmed-meshheading:7708776-Cytosol,
pubmed-meshheading:7708776-Evoked Potentials,
pubmed-meshheading:7708776-Exocytosis,
pubmed-meshheading:7708776-Kinetics,
pubmed-meshheading:7708776-Membrane Potentials,
pubmed-meshheading:7708776-Nicotine,
pubmed-meshheading:7708776-Patch-Clamp Techniques,
pubmed-meshheading:7708776-Receptors, Nicotinic,
pubmed-meshheading:7708776-Terpenes,
pubmed-meshheading:7708776-Thapsigargin,
pubmed-meshheading:7708776-Time Factors,
pubmed-meshheading:7708776-Tubocurarine
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pubmed:year |
1995
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pubmed:articleTitle |
Activation of nicotinic receptors triggers exocytosis from bovine chromaffin cells in the absence of membrane depolarization.
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pubmed:affiliation |
Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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