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dc.contributor.authorD'Adamo, M.C.*
dc.contributor.authorShang, Lijun*
dc.contributor.authorImbrici, P.*
dc.contributor.authorBrown, S.D.M.*
dc.contributor.authorPessia, M.*
dc.contributor.authorTucker, S.J.*
dc.date.accessioned2014-04-25T14:55:01Z
dc.date.available2014-04-25T14:55:01Z
dc.date.issued2011
dc.identifier.citationD'Adamo MC, Shang L, Imbrici P, Brown SD, Pessia M and Tucker SJ (2011) Genetic inactivation of Kcnj16 identifies Kir5.1 as an important determinant of neuronal PCO2/pH sensitivity. Journal of Biological Chemistry. 286(1): 192-198.
dc.identifier.urihttp://hdl.handle.net/10454/5950
dc.descriptionNo
dc.description.abstractThe molecular identity of ion channels which confer PCO(2)/pH sensitivity in the brain is unclear. Heteromeric Kir4.1/Kir5.1 channels are highly sensitive to inhibition by intracellular pH and are widely expressed in several brainstem nuclei involved in cardiorespiratory control, including the locus coeruleus. This has therefore led to a proposed role for these channels in neuronal CO(2) chemosensitivity. To examine this, we generated mutant mice lacking the Kir5.1 (Kcnj16) gene. We show that although locus coeruleus neurons from Kcnj16((+/+)) mice rapidly respond to cytoplasmic alkalinization and acidification, those from Kcnj16((-/-)) mice display a dramatically reduced and delayed response. These results identify Kir5.1 as an important determinant of PCO(2)/pH sensitivity in locus coeruleus neurons and suggest that Kir5.1 may be involved in the response to hypercapnic acidosis.
dc.relation.isreferencedbyhttp://dx.doi.org/10.1074/jbc.M110.189290
dc.subjectAcidosis
dc.subject; Animals
dc.subject; Carbon dioxide
dc.subject; Electric conductivity
dc.subject; Female
dc.subject; Gene deletion
dc.subject; Hydrogen-ion concentration
dc.subject; Locus coeruleus
dc.subject; Male
dc.subject; Mice; Inbred C57BL
dc.subject; Neurons
dc.subject; Potassium channels
dc.subject; REF 2014
dc.titleGenetic inactivation of Kcnj16 identifies Kir5.1 as an important determinant of neuronal PCO2/pH sensitivity
dc.status.refereedYes
dc.typeArticle
dc.type.versionNo full-text in the repository


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