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000005103 0247_ $$2DOI$$a10.1523/JNEUROSCI.0689-09.2009
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000005103 084__ $$2WoS$$aNeurosciences
000005103 1001_ $$0P:(DE-HGF)0$$aKanyshkova, T.$$b0
000005103 245__ $$aPostnatal expression pattern of HCN channel isoforms in thalamic neurons: Relationship to maturation of thalamocortical oscillations
000005103 260__ $$aWashington, DC$$bSoc.$$c2009
000005103 300__ $$a8857 - 8847
000005103 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article
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000005103 3367_ $$2BibTeX$$aARTICLE
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000005103 3367_ $$2DRIVER$$aarticle
000005103 440_0 $$03603$$aJournal of Neuroscience$$v29$$x0270-6474$$y27
000005103 500__ $$aThis work was supported by Deutsche Forschungsgemeinschaft Grants BU 1019/8-1 and BE 4107/2-1, Interdisziplinares Zentrum fur Klinische Forschung Grant Bud/005/07, and National Institutes of Health Grants NS 35439 and NS 45540. This work was done in partial fulfillment of the MD thesis of M. P. and the PhD thesis of P. M. We thank A. Markovic, E. Nass, and S. Ruppel for excellent technical assistance.
000005103 520__ $$aHyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels are the molecular substrate of the hyperpolarization-activated inward current (I(h)). Because the developmental profile of HCN channels in the thalamus is not well understood, we combined electrophysiological, molecular, immunohistochemical, EEG recordings in vivo, and computer modeling techniques to examine HCN gene expression and I(h) properties in rat thalamocortical relay (TC) neurons in the dorsal part of the lateral geniculate nucleus and the functional consequence of this maturation. Recordings of TC neurons revealed an approximate sixfold increase in I(h) density between postnatal day 3 (P3) and P106, which was accompanied by significantly altered current kinetics, cAMP sensitivity, and steady-state activation properties. Quantification on tissue levels revealed a significant developmental decrease in cAMP. Consequently the block of basal adenylyl cyclase activity was accompanied by a hyperpolarizing shift of the I(h) activation curve in young but not adult rats. Quantitative analyses of HCN channel isoforms revealed a steady increase of mRNA and protein expression levels of HCN1, HCN2, and HCN4 with reduced relative abundance of HCN4. Computer modeling in a simplified thalamic network indicated that the occurrence of rhythmic delta activity, which was present in the EEG at P12, differentially depended on I(h) conductance and modulation by cAMP at different developmental states. These data indicate that the developmental increase in I(h) density results from increased expression of three HCN channel isoforms and that isoform composition and intracellular cAMP levels interact in determining I(h) properties to enable progressive maturation of rhythmic slow-wave sleep activity patterns.
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000005103 650_2 $$2MeSH$$aAnimals
000005103 650_2 $$2MeSH$$aAnimals, Newborn
000005103 650_2 $$2MeSH$$aBiological Clocks: physiology
000005103 650_2 $$2MeSH$$aCerebral Cortex: growth & development
000005103 650_2 $$2MeSH$$aCerebral Cortex: metabolism
000005103 650_2 $$2MeSH$$aCyclic Nucleotide-Gated Cation Channels: biosynthesis
000005103 650_2 $$2MeSH$$aCyclic Nucleotide-Gated Cation Channels: genetics
000005103 650_2 $$2MeSH$$aGene Expression Regulation, Developmental: physiology
000005103 650_2 $$2MeSH$$aIon Channels: biosynthesis
000005103 650_2 $$2MeSH$$aIon Channels: genetics
000005103 650_2 $$2MeSH$$aNeural Pathways: growth & development
000005103 650_2 $$2MeSH$$aNeural Pathways: metabolism
000005103 650_2 $$2MeSH$$aNeurons: metabolism
000005103 650_2 $$2MeSH$$aNeurons: physiology
000005103 650_2 $$2MeSH$$aPotassium Channels: biosynthesis
000005103 650_2 $$2MeSH$$aPotassium Channels: genetics
000005103 650_2 $$2MeSH$$aProtein Isoforms: biosynthesis
000005103 650_2 $$2MeSH$$aRats
000005103 650_2 $$2MeSH$$aRats, Sprague-Dawley
000005103 650_2 $$2MeSH$$aThalamus: growth & development
000005103 650_2 $$2MeSH$$aThalamus: metabolism
000005103 650_7 $$00$$2NLM Chemicals$$aCyclic Nucleotide-Gated Cation Channels
000005103 650_7 $$00$$2NLM Chemicals$$aHCN2 potassium channel
000005103 650_7 $$00$$2NLM Chemicals$$aHCN3 protein, rat
000005103 650_7 $$00$$2NLM Chemicals$$aHCN4 protein, rat
000005103 650_7 $$00$$2NLM Chemicals$$aIon Channels
000005103 650_7 $$00$$2NLM Chemicals$$aPotassium Channels
000005103 650_7 $$00$$2NLM Chemicals$$aProtein Isoforms
000005103 650_7 $$00$$2NLM Chemicals$$ahyperpolarization-activated cation channel
000005103 650_7 $$2WoSType$$aJ
000005103 7001_ $$0P:(DE-HGF)0$$aPawlowski, M.$$b1
000005103 7001_ $$0P:(DE-HGF)0$$aMeuth, P.$$b2
000005103 7001_ $$0P:(DE-HGF)0$$aDube, C.$$b3
000005103 7001_ $$0P:(DE-HGF)0$$aBender, R. A.$$b4
000005103 7001_ $$0P:(DE-HGF)0$$aBrewster, A. L..$$b5
000005103 7001_ $$0P:(DE-Juel1)131911$$aBaumann, A.$$b6$$uFZJ
000005103 7001_ $$0P:(DE-HGF)0$$aBaram, T. Z.$$b7
000005103 7001_ $$0P:(DE-HGF)0$$aPape, H.-C.$$b8
000005103 7001_ $$0P:(DE-HGF)0$$aBudde, T.$$b9
000005103 773__ $$0PERI:(DE-600)1475274-8$$a10.1523/JNEUROSCI.0689-09.2009$$gVol. 29, p. 8857 - 8847$$p8857 - 8847$$q29<8857 - 8847$$tThe @journal of neuroscience$$v29$$x0270-6474$$y2009
000005103 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768285
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