uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Mechanisms of nicotine mediated communication between NGF-differentiated PC12 and HEL cells
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Neuroscience.
2002 In: Neuroreport, ISSN 0959-4965, Vol. 13, no 9, 1157-1161 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2002. Vol. 13, no 9, 1157-1161 p.
Identifiers
URN: urn:nbn:se:uu:diva-91901OAI: oai:DiVA.org:uu-91901DiVA: diva2:164778
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.
Series
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1361
Keyword
Physiology, calcium, neurotransmitter release, nicotine, depolarization, G-protein coupled receptor, muscarinic, phospholipase C, m-3M3FBS, Fysiologi
National Category
Physiology
Identifiers
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
Opponent
Supervisors
Available from: 2004-05-12 Created: 2004-05-12Bibliographically approved

Open Access in DiVA

No full text

By organisation
Department of Neuroscience

Search outside of DiVA

GoogleGoogle Scholar

urn-nbn

Altmetric score

urn-nbn
Total: 356 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf