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Functional characterization of mouse α4β2 nicotinic acetylcholine receptors stably expressed in HEK293T cells
dc.contributor.authorKaradsheh, Mark S.en_US
dc.contributor.authorShah, M. Salmanen_US
dc.contributor.authorTang, Xinen_US
dc.contributor.authorMacdonald, Robert L.en_US
dc.contributor.authorStitzel, Jerry A.en_US
dc.date.accessioned2010-04-01T14:46:55Z
dc.date.available2010-04-01T14:46:55Z
dc.date.issued2004-12en_US
dc.identifier.citationKaradsheh, Mark S.; Shah, M. Salman; Tang, Xin; Macdonald, Robert L.; Stitzel, Jerry A. (2004). "Functional characterization of mouse α4β2 nicotinic acetylcholine receptors stably expressed in HEK293T cells." Journal of Neurochemistry 91(5): 1138-1150. <http://hdl.handle.net/2027.42/65230>en_US
dc.identifier.issn0022-3042en_US
dc.identifier.issn1471-4159en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/65230
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15569257&dopt=citationen_US
dc.description.abstractMouse α4β2 nicotinic acetylcholine receptors (nAchRs) were stably expressed in HEK293T cells. The function of this stable cell line, termed mmα4β2, was assessed using an aequorin-based luminescence method that measures agonist-evoked changes in intracellular calcium. Agonist-elicited changes in intracellular calcium were due primarily to direct entry of calcium through the α4β2 channel, although release of calcium from intracellular stores contributed ˜ 28% of the agonist-evoked response. Agonist pharmacologies were very similar between the mmα4β2 cells and most cell lines that stably express human α4β2 nAchRs. Based on agonist profiles and sensitivity to the antagonist dihydro-β-erythroidine (DHβE), the predominant α4β2 nAchR expressed in the mmα4β2 cells exhibits a pharmacology that most resembles the DHβE-sensitive component of 86 Rb + efflux from mouse brain synaptosomes. However, when evaluated with the aequorin assay, the mmα4β2 nAchR was found to be atypically sensitive to blockade by the presumed α7-selective antagonist methyllycaconitine (MLA), exhibiting an IC 50 value of 31 ± 0.1 nm. Similar IC 50 values have been reported for the MLA inhibition of nicotine-stimulated dopamine release, a response that is mediated by β2-subunit-containing nAchRs and not α7-subunit-containing nAchRs. Consequently, at low nanomolar concentrations, MLA may not be as selective for α7-containing nAchRs as previously thought.en_US
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dc.format.extent3110 bytes
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dc.publisherBlackwell Science Ltden_US
dc.rights2004 International Society for Neurochemistryen_US
dc.subject.otherAequorinen_US
dc.subject.otherCalciumen_US
dc.subject.otherHeterologous Expressionen_US
dc.subject.otherLuminescenceen_US
dc.subject.otherMethyllycaconitineen_US
dc.titleFunctional characterization of mouse α4β2 nicotinic acetylcholine receptors stably expressed in HEK293T cellsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum* Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationother† Department of Neurology, Vanderbilt University Medical School, Nashville, Tennessee, USAen_US
dc.contributor.affiliationother† Department of Integrative Physiology and Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, USAen_US
dc.identifier.pmid15569257en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/65230/1/j.1471-4159.2004.02801.x.pdf
dc.identifier.doi10.1111/j.1471-4159.2004.02801.xen_US
dc.identifier.sourceJournal of Neurochemistryen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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