| pubmed-article:7708776 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C0007452 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C0376604 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C0015283 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C0034830 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C0332197 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C1816453 | lld:lifeskim |
| pubmed-article:7708776 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7708776 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:7708776 | pubmed:dateCreated | 1995-5-11 | lld:pubmed |
| pubmed-article:7708776 | 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. | lld:pubmed |
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| pubmed-article:7708776 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7708776 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7708776 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7708776 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7708776 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:7708776 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:7708776 | pubmed:author | pubmed-author:NowyckyM CMC | lld:pubmed |
| pubmed-article:7708776 | pubmed:author | pubmed-author:MollardPP | lld:pubmed |
| pubmed-article:7708776 | pubmed:author | pubmed-author:SewardE PEP | lld:pubmed |
| pubmed-article:7708776 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7708776 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:7708776 | pubmed:volume | 92 | lld:pubmed |
| pubmed-article:7708776 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7708776 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7708776 | pubmed:pagination | 3065-9 | lld:pubmed |
| pubmed-article:7708776 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:7708776 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7708776 | pubmed:articleTitle | Activation of nicotinic receptors triggers exocytosis from bovine chromaffin cells in the absence of membrane depolarization. | lld:pubmed |
| pubmed-article:7708776 | pubmed:affiliation | Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129, USA. | lld:pubmed |
| pubmed-article:7708776 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7708776 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7708776 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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