Reference : Nuclear calcium signaling in spinal neurons drives a genomic program required for per...

	Document type :	Scientific journals : Article
	Discipline(s) :	Life sciences : Multidisciplinary, general & others
	To cite this reference:	http://hdl.handle.net/10993/26568

Title :	Nuclear calcium signaling in spinal neurons drives a genomic program required for persistent inflammatory pain
Language :	English
Author, co-author :	Simonetti, Manuela [University of Heidelberg > Institute for Pharmacology]
	Hagenston, Anna [Interdisciplinary Center for Neurosciences, University of Heidelberg > Department of Neurobiology]
	Vardeh, Daniel [University of Heidelberg > Institute for Pharmacology]
	Freitag, Eckehard [Interdisciplinary Center for Neurosciences, University of Heidelberg > Department of Neurobiology]
	Mauceri, Daniela [Interdisciplinary Center for Neurosciences, University of Heidelberg > Department of Neurobiology]
	Lu, Jianning [University of Heidelberg > Institute for Pharmacology]
	Satagopam, Venkata [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > >]
	Schneider, Reinhard [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > > ; European Molecular Biology Laboratory (EMBL) > 3Structural and Computational Biology Unit]
	Costigan, Michael [Children’s Hospital Boston and Harvard Medical School > F.M. Kirby Neurobiology Center]
	Bading, Hilmar [Interdisciplinary Center for Neurosciences, University of Heidelberg > Department of Neurobiology]
	Kuner, Rohini [University of Heidelberg > Institute for Pharmacology]
Publication date :	2013
Journal title :	Neuron
Publisher :	Cell Press
Volume :	77
Issue/season :	1
Pages :	43-57
Peer reviewed :	Yes (verified by ORBilu)
ISSN :	0896-6273
e-ISSN :	1097-4199
City :	Cambridge
Country :	United Kingdom
Abstract :	[en] Persistent pain induced by noxious stimuli is characterized by the transition from normosensitivity to hypersensitivity. Underlying mechanisms are not well understood, although gene expression is considered important. Here we show that persistent nociceptive-like activity triggers calcium transients in neuronal nuclei within the superficial spinal dorsal horn, and that nuclear calcium is necessary for the development of long-term inflammatory hypersensitivity. Using a nucleusspecific calcium signal perturbation strategy in vivo complemented by gene profiling, bioinformatics and functional analyses, we discovered a pain-associated, nuclear calciumregulated gene program in spinal excitatory neurons. This includes C1q, a novel modulator of synaptic spine morphogenesis, which we found to contribute to activity-dependent spine remodelling on spinal neurons in a manner functionally associated with inflammatory hypersensitivity. Thus, nuclear calcium integrates synapse-to-nucleus communication following noxious stimulation and controls a spinal genomic response that mediates the transition between acute and long-term nociceptive sensitization by modulating functional and structural plasticity.
Research centres :	Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group)
Permalink :	http://hdl.handle.net/10993/26568
DOI :	10.1016/j.neuron.2012.10.037

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