title: Massive normalization of olfactory bulb output in mice with a 'monoclonal nose'.
abstract: Perturbations in neural circuits can provide mechanistic understanding of the neural correlates of behavior. In M71 transgenic mice with a "monoclonal nose", glomerular input patterns in the olfactory bulb are massively perturbed and olfactory behaviors are altered. To gain insights into how olfactory circuits can process such degraded inputs we characterized odor-evoked responses of olfactory bulb mitral cells and interneurons. Surprisingly, calcium imaging experiments reveal that mitral cell responses in M71 transgenic mice are largely normal, highlighting a remarkable capacity of olfactory circuits to normalize sensory input. In vivo whole cell recordings suggest that feedforward inhibition from olfactory bulb periglomerular cells can mediate this signal normalization. Together, our results identify inhibitory circuits in the olfactory bulb as a mechanistic basis for many of the behavioral phenotypes of mice with a "monoclonal nose" and highlight how substantially degraded odor input can be transformed to yield meaningful olfactory bulb output.
authors.affiliation: Center for Interdisciplinary Research in Biology, Collège de France, INSERM U1050, CNRS UMR 7241, Paris, France.
authors.forename: Benjamin
authors.initials: B
authors.lastname: Roland
authors.affiliation: The Francis Crick Institute, London, United Kingdom.|Department of Neuroscience, Physiology and Pharmacology, University College London, London, United Kingdom.
authors.forename: Rebecca
authors.initials: R
authors.lastname: Jordan
authors.affiliation: Wolfson Institute for Biomedical Research, University College London, London, United Kingdom.
authors.forename: Dara L
authors.initials: DL
authors.lastname: Sosulski
authors.affiliation: Center for Interdisciplinary Research in Biology, Collège de France, INSERM U1050, CNRS UMR 7241, Paris, France.
authors.forename: Assunta
authors.initials: A
authors.lastname: Diodato
authors.affiliation: The Francis Crick Institute, London, United Kingdom.|Behavioural Neurophysiology, Max-Planck-Institute for Medical Research, Heidelberg, Germany.
authors.forename: Izumi
authors.initials: I
authors.lastname: Fukunaga
authors.affiliation: MIT Genetic Neuroengineering Group, McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, United States.
authors.forename: Ian
authors.initials: I
authors.lastname: Wickersham
authors.affiliation: Department of Neurobiology, Duke University, Durham, United States.
authors.forename: Kevin M
authors.initials: KM
authors.lastname: Franks
authors.affiliation: The Francis Crick Institute, London, United Kingdom.|Department of Neuroscience, Physiology and Pharmacology, University College London, London, United Kingdom.|Behavioural Neurophysiology, Max-Planck-Institute for Medical Research, Heidelberg, Germany.|Department of Anatomy and Cell Biology, Faculty of Medicine, University of Heidelberg, Heidelberg, Germany.
authors.forename: Andreas T
authors.initials: AT
authors.lastname: Schaefer
authors.affiliation: Center for Interdisciplinary Research in Biology, Collège de France, INSERM U1050, CNRS UMR 7241, Paris, France.
authors.forename: Alexander
authors.identifier: 0000-0001-7956-9096
authors.initials: A
authors.lastname: Fleischmann
mesh_terms: D000818:Animals; D008822:Mice, Transgenic; D009415:Nerve Net / Q000502:physiology* / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D000857:Olfaction Disorders / Q000235:genetics; D009830:Olfactory Bulb / Q000502:physiology* / Q000503:physiopathology*
keywords: excitation/inhibition balance; mouse; neuroscience; olfaction; olfactory bulb; signal normalization