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Reconstitution of neurotransmission by determining communication between differentiated PC12 pheochromocytoma and HEL 92.1.7 erythroleukemia cells
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Neuroscience.
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2001 In: Pflugers Archiv, ISSN 0031-6768, Vol. 442, no 2, 312-320 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2001. Vol. 442, no 2, 312-320 p.
URN: urn:nbn:se:uu:diva-91902OAI: oai:DiVA.org:uu-91902DiVA: diva2:164779
Available from: 2004-05-12 Created: 2004-05-12Bibliographically approved
In thesis
1. Investigation on Pre- and Postsynaptic Ca2+ Signaling in Neuronal Model Systems
Open this publication in new window or tab >>Investigation on Pre- and Postsynaptic Ca2+ Signaling in Neuronal Model Systems
2004 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Communication between neuronal and non-neuronal is called volume transmission when the released neurotransmitter (NT) acts via diffusion and affects several target cells. Both the neurosecretory and postsynaptic cell responses are linked to [Ca2+]i elevations.

In the present thesis the role of pre-and postsynaptic Ca2+ elevations has been investigated in the reconstituted "synapse" model comprised of NGF-differentiated PC12 and HEL cells as well as in SH-SY5Y neuroblastoma cells. In PC12 cells, both 70mM K+ and nicotine triggered NT release, which could be detected as a secondary [Ca2+]i increase in surrounding HEL cells. Both secretagogues shared the same voltage-dependent Ca2+ influx pathway as judged from the pharmacological profile blockers of voltage-gated Ca2+ channels. The coupling of electrical responses to the activation of Ca2+ signaling via muscarinic receptors in SH-SY5Y cells was also studied. These data revealed that depolarization caused a considerable potentiation of the muscarinic Ca2+ response. The potentiated Ca2+ increase was mainly dependent on the enhanced Ca2+ influx and to a lesser extent on [Ca2+]i release from intracellular stores. A phospholipase C (PLC) activator, m-3M3FBS was used to further study the role of G-protein coupled receptor (GPCR)-coupled Ca2+ signaling. However, it was found that m-3M3FBS instead triggered [Ca2+]i elevations independently of PLC activation.

In conclusion, the results indicate that the magnitude of NT release from PC12 cells is sufficient to cause a robust activation of neighboring target cells. Postsynaptic muscarinic signaling is amplified due to integration of electrical excitation and GPCR signaling. The PLC activator, m-3M3FBS is not suitable for studies of PLC-mediated signals in intact cells.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2004. 52 p.
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1361
Physiology, calcium, neurotransmitter release, nicotine, depolarization, G-protein coupled receptor, muscarinic, phospholipase C, m-3M3FBS, Fysiologi
National Category
urn:nbn:se:uu:diva-4300 (URN)91-554-5993-5 (ISBN)
Public defence
2004-06-05, Room B21, BMC, Husargatan 3, Uppsala, 09:15
Available from: 2004-05-12 Created: 2004-05-12Bibliographically approved

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