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Characterization of $Ca^{2+}$signaling pathways in mouse adrenal medullary chromaffin cells
| Content Provider | Scilit |
|---|---|
| Author | Wu, Pei-Chun Fann, Ming-Ji Kao, Lung-Sen |
| Copyright Year | 2010 |
| Description | Journal: Journal of Neurochemistry In the present study, we characterized the Ca2+ responses and secretions induced by various secretagogues in mouse chromaffin cells. Activation of the acetylcholine receptor (AChR) by carbachol induced a transient intracellular Ca2+ concentration ([Ca2+](i)) increase followed by two phases of [Ca2+](i) decay and a burst of exocytic events. The contribution of the subtypes of AChRs to carbachol-induced responses was examined. Based on the results obtained by stimulating the cells with the nicotinic receptor (nAChR) agonist, 1,1-dimethyl-4-phenylpiperazinium iodide, high K(+) and the effects of thapsigargin, it appears that activation of nAChRs induces an extracellular Ca2+ influx, which in turn activate Ca(2+)-induced Ca2+ release via the ryanodine receptors. Muscarine, a muscarinic receptor (mAChRs) agonist, was found to induce [Ca2+](i) oscillation and sustained catecholamine release, possibly by activation of both the receptor- and store-operated Ca2+ entry pathways. The RT-PCR results showed that mouse chromaffin cells are equipped with messages for multiple subtypes of AChRs, ryanodine receptors and all known components of the receptor- and store-operated Ca2+ entry. Furthermore, results obtained by directly monitoring endoplasmic reticulum (ER) and mitochondrial Ca2+ concentration and by disabling mitochondrial Ca2+ uptake suggest that the ER acts as a Ca2+ source, while the mitochondria acts as a Ca2+ sink. Our results show that both nAChRs and mAChRs contribute to the initial carbachol-induced [Ca2+](i) increase which is further enhanced by the Ca2+ released from the ER mediated by Ca(2+)-induced Ca2+ release and mAChR activation. This information on the Ca2+ signaling pathways should lay a good foundation for future studies using mouse chromaffin cells as a model system. |
| Related Links | http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2009.06533.x/pdf |
| Ending Page | 1222 |
| Page Count | 13 |
| Starting Page | 1210 |
| e-ISSN | 14714159 |
| DOI | 10.1111/j.1471-4159.2009.06533.x |
| Journal | Journal of Neurochemistry |
| Issue Number | 5 |
| Volume Number | 112 |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 2010-03-01 |
| Access Restriction | Open |
| Subject Keyword | Journal: Journal of Neurochemistry Endoplasmic Reticulum |
| Content Type | Text |
| Resource Type | Article |
