dc.contributor.author
Barthel, Lennart
dc.contributor.author
Reetz, Olivia
dc.contributor.author
Strauss, Ulf
dc.date.accessioned
2018-06-08T03:18:50Z
dc.date.available
2016-07-15T12:31:53.137Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/14900
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-19088
dc.description.abstract
Background/Aims: Cationic currents (Ih) through the fast activating and
relatively cAMP insensitive subtype of hyperpolarization-activated cyclic
nucleotide-gated (HCN) channels, HCN1, are limited by cytosolic factors in
mammalian cells. This cytosolic HCN1 break is boosted by changes in membrane
voltage that are not characterized on a biophysical level, yet. Methods: We
overexpressed rat (r)HCN1 in human embryonic kidney cells (HEK293) and
recorded pharmacologically isolated Ih in cell-attached or whole-cell mode of
the patch-clamp technique. Results: Recurring activation of rHCN1 reduced and
slowed Ih in intact HEK293 cells (cell-attached mode). On the contrary,
sustained disruption of the intracellular content (whole-cell mode) ceased
activity dependence and partially enables voltage dependent hysteresis. The
activity induced Ih attenuation in intact cells was independent of the main
external cation, depended on the number of previous forced activations and was
- at least in part - due to a shift in the voltage dependence of activation
towards hyperpolarization as estimated by an adapted tail current analysis.
Intracellular elevation of cAMP could not reverse the changes in Ih.
Conclusion: Reduction of rHCN1 mediated Ih is use dependent and may involve
the coupling of voltage sensor and pore.
en
dc.rights.uri
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Use Dependent Attenuation of Rat HCN1-Mediated Ih in Intact HEK293 Cells
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Cell Physiol Biochem. - 38 (2016), 6, S. 2079-2093
dcterms.bibliographicCitation.doi
10.1159/000445566
dcterms.bibliographicCitation.url
http://www.karger.com/Article/FullText/445566
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000025010
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000006782
dcterms.accessRights.openaire
open access