TY - JOUR
AU - Knop, G.C.
AU - Seeliger, M.W.
AU - Thiel, F.
AU - Mataruga, A.
AU - Kaupp, U. B.
AU - Friedburg, C.
AU - Tanimoto, N.
AU - Müller, F.
TI - Light responses in the mouse retina are prolonged upon targeted deletion of the HCN1 channel gene
JO - European journal of neuroscience
VL - 28
SN - 0953-816X
CY - Oxford [u.a.]
PB - Blackwell
M1 - PreJuSER-1483
SP - 2221 - 2230
PY - 2008
N1 - We thank Dr Eric Kandel ( Columbia University, USA) for providing the HCN1 knock-out line, Christoph Aretzweiler for technical assistance in immunohistochemistry and genotyping of HCN1 knock-out animals, Mechthilde Bruns for help in cell culture, and Dr Wolfgang Bonigk for the cDNA of murine HCN1. M. W. Seeliger was supported by the Deutsche Forschungsgemeinschaft ( DFG Se837/4-1 and Se837/5-1).
AB - 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.
KW - Amacrine Cells: metabolism
KW - Amacrine Cells: radiation effects
KW - Animals
KW - Cyclic Nucleotide-Gated Cation Channels: genetics
KW - Electroretinography
KW - Immunohistochemistry
KW - Membrane Potentials: genetics
KW - Membrane Potentials: radiation effects
KW - Mice
KW - Mice, Inbred C57BL
KW - Mice, Knockout
KW - Neurons: metabolism
KW - Neurons: radiation effects
KW - Organ Culture Techniques
KW - Patch-Clamp Techniques
KW - Photic Stimulation
KW - Photoreceptor Cells, Vertebrate: metabolism
KW - Photoreceptor Cells, Vertebrate: radiation effects
KW - Potassium Channels: genetics
KW - Retina: metabolism
KW - Retina: radiation effects
KW - Retinal Bipolar Cells: metabolism
KW - Retinal Bipolar Cells: radiation effects
KW - Retinal Ganglion Cells: metabolism
KW - Retinal Ganglion Cells: radiation effects
KW - Synaptic Transmission: genetics
KW - Synaptic Transmission: radiation effects
KW - Vision, Ocular: genetics
KW - Cyclic Nucleotide-Gated Cation Channels (NLM Chemicals)
KW - Potassium Channels (NLM Chemicals)
KW - hyperpolarization-activated cation channel (NLM Chemicals)
KW - J (WoSType)
LB - PUB:(DE-HGF)16
C6 - pmid:19019198
UR - <Go to ISI:>//WOS:000261184800006
DO - DOI:10.1111/j.1460-9568.2008.06512.x
UR - https://juser.fz-juelich.de/record/1483
ER -