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@ARTICLE{Mobley:14281,
      author       = {Mobley, A.S. and Miller, A.M. and Araneda, R.C. and Maurer,
                      L.R. and Müller, F. and Greer, C.A.},
      title        = {{H}yperpolarization-activated cyclic nucleotide-gated
                      channels in olfactory sensory neurons regulate axon
                      extension and glomerular formation},
      journal      = {The journal of neuroscience},
      volume       = {30},
      issn         = {0270-6474},
      address      = {Washington, DC},
      publisher    = {Soc.},
      reportid     = {PreJuSER-14281},
      pages        = {16498 - 16508},
      year         = {2010},
      note         = {This work was funded by National Institutes of Health
                      (NIH)-National Institute on Deafness and Other Communication
                      Disorders and NIH-National Institute on Aging grants
                      (C.A.G.). A.M.M. was supported by Medical Scientist Training
                      Program Grant GM07205 and NIH Grant F30 DC010324. A.S.M. was
                      supported by Neurobiology Training Grant NS 007224-24 and
                      National Research Service Award F32 DC010098-01A1. We thank
                      Drs. L. Rela and M. B. Richard for developing the
                      whole-mount imaging technique in our lab. HCN antibodies
                      were generously provided by Dr. R. Shigemoto, National
                      Institute for Physiological Sciences, Japan.},
      abstract     = {Mechanisms influencing the development of olfactory bulb
                      glomeruli are poorly understood. While odor receptors (ORs)
                      play an important role in olfactory sensory neuron (OSN)
                      axon targeting/coalescence (Mombaerts et al., 1996; Wang et
                      al., 1998; Feinstein and Mombaerts, 2004), recent work
                      showed that G protein activation alone is sufficient to
                      induce OSN axon coalescence (Imai et al., 2006; Chesler et
                      al., 2007), suggesting an activity-dependent mechanism in
                      glomerular development. Consistent with these data, OSN axon
                      projections and convergence are perturbed in mice deficient
                      for adenylyl cyclase III, which is downstream from the OR
                      and catalyzes the conversion of ATP to cAMP. However, in
                      cyclic nucleotide-gated (CNG) channel knock-out mice OSN
                      axons are only transiently perturbed (Lin et al., 2000),
                      suggesting that the CNG channel may not be the sole target
                      of cAMP. This prompted us to investigate an alternative
                      channel, the hyperpolarization-activated, cyclic
                      nucleotide-gated cation channel (HCN), as a potential
                      developmental target of cAMP in OSNs. Here, we demonstrate
                      that HCN channels are developmentally precocious in OSNs and
                      therefore are plausible candidates for affecting OSN axon
                      development. Inhibition of HCN channels in dissociated OSNs
                      significantly reduced neurite outgrowth. Moreover, in HCN1
                      knock-out mice the formation of glomeruli was delayed in
                      parallel with perturbations of axon organization in the
                      olfactory nerve. These data support the hypothesis that the
                      outgrowth and coalescence of OSN axons is, at least in part,
                      subject to activity-dependent mechanisms mediated via HCN
                      channels.},
      keywords     = {Animals / Animals, Newborn / Antidiarrheals: pharmacology /
                      Axons: drug effects / Axons: physiology / Biophysics:
                      methods / Cardiotonic Agents: pharmacology / Cells, Cultured
                      / Cyclic Nucleotide-Gated Cation Channels: deficiency /
                      Cyclic Nucleotide-Gated Cation Channels: physiology /
                      Electric Stimulation: methods / Embryo, Mammalian / GAP-43
                      Protein: metabolism / Gene Expression Regulation,
                      Developmental: drug effects / Gene Expression Regulation,
                      Developmental: physiology / Green Fluorescent Proteins:
                      genetics / Ion Channels: genetics / Ion Channels: metabolism
                      / Loperamide: pharmacology / Membrane Potentials: drug
                      effects / Membrane Potentials: genetics / Mice / Mice,
                      Inbred C57BL / Mice, Knockout / Neural Cell Adhesion
                      Molecules: metabolism / Neurogenesis: drug effects /
                      Neurogenesis: physiology / Olfactory Bulb: cytology /
                      Olfactory Bulb: embryology / Olfactory Bulb: growth $\&$
                      development / Patch-Clamp Techniques: methods / Potassium
                      Channels: deficiency / Potassium Channels: genetics /
                      Potassium Channels: metabolism / Potassium Channels:
                      physiology / Pyrimidines: pharmacology / Receptors, Odorant:
                      genetics / Receptors, Odorant: metabolism / Sensory Receptor
                      Cells: cytology / Sensory Receptor Cells: drug effects /
                      Antidiarrheals (NLM Chemicals) / Cardiotonic Agents (NLM
                      Chemicals) / Cyclic Nucleotide-Gated Cation Channels (NLM
                      Chemicals) / GAP-43 Protein (NLM Chemicals) / HCN2 potassium
                      channel (NLM Chemicals) / HCN4 protein, rat (NLM Chemicals)
                      / Ion Channels (NLM Chemicals) / Neural Cell Adhesion
                      Molecules (NLM Chemicals) / Olfr1507 protein, mouse (NLM
                      Chemicals) / Potassium Channels (NLM Chemicals) /
                      Pyrimidines (NLM Chemicals) / Receptors, Odorant (NLM
                      Chemicals) / hyperpolarization-activated cation channel (NLM
                      Chemicals) / ICI D2788 (NLM Chemicals) / Green Fluorescent
                      Proteins (NLM Chemicals) / Loperamide (NLM Chemicals) / J
                      (WoSType)},
      cin          = {ISB-1},
      ddc          = {590},
      cid          = {I:(DE-Juel1)VDB922},
      pnm          = {BioSoft: Makromolekulare Systeme und biologische
                      Informationsverarbeitung},
      pid          = {G:(DE-Juel1)FUEK505},
      shelfmark    = {Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21147989},
      pmc          = {pmc:PMC3393111},
      UT           = {WOS:000285089100011},
      doi          = {10.1523/JNEUROSCI.4225-10.2010},
      url          = {https://juser.fz-juelich.de/record/14281},
}