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  Light responses in the mouse retina are prolonged upon targeted deletion of the HCN1 channel gene

Knop, G. C., Seeliger, M. W., Thiel, F., Mataruga, A., Kaupp, U. B., Friedburg, C., et al. (2008). Light responses in the mouse retina are prolonged upon targeted deletion of the HCN1 channel gene. European Jorunal of Neuroscience, 28(11), 2221-2230.

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Knop, G. C., Autor
Seeliger, M. W., Autor
Thiel, F., Autor
Mataruga, A., Autor
Kaupp, U. B.1, Autor
Friedburg, C., Autor
Tanimoto, N., Autor
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1External Organizations, ou_persistent22              

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 Zusammenfassung: Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels contribute to pacemaker activity, and co-determine the integrative behaviour of neurons and shape their response to synaptic stimulation. Four channel isoforms, HCN1-4, have been described in mammals. Recent studies showed particularly strong expression of HCN1 channels in rods and cones of the rat retina, suggesting that HCN1 channels are involved in the shaping of light responses in both types of photoreceptors. Therefore, the loss of HCN1 channels should lead to pronounced changes in light-induced electrical responses under both scotopic and photopic conditions. This was tested using a mouse transgenic approach. We used immunohistochemistry and patch-clamp recording to study the distribution of HCN1 channels in the mouse retina. HCN1 channels were strongly expressed in rod and cone photoreceptors, as well as in some bipolar, amacrine and ganglion cell types. In electroretinograms (ERGs) from animals in which the HCN1 channel gene had been knocked out, the b-wave amplitudes were unaltered (scotopic conditions) or somewhat reduced (photopic conditions), whereas the duration of both scotopic and photopic ERG responses was strikingly prolonged. Our data suggest that in visual information processing, shortening and shaping of light responses by activation of HCN1 at the level of the photoreceptors is an important step in both scotopic and photopic pathways

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 Datum: 2008
 Publikationsstatus: Erschienen
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 Identifikatoren: ISI: ISI:000261184800006
ISSN: 0953-816X
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Titel: European Jorunal of Neuroscience
  Alternativer Titel : Eur.J.Neurosci.
Genre der Quelle: Zeitschrift
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Seiten: - Band / Heft: 28 (11) Artikelnummer: - Start- / Endseite: 2221 - 2230 Identifikator: -