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Nat Commun. 2015 Apr 13;6:6820. doi: 10.1038/ncomms7820.

A role for Kalirin-7 in nociceptive sensitization via activity-dependent modulation of spinal synapses.

Author information

1
Department of Molecular Pharmacology, Pharmacology Institute, Medical Faculty Heidelberg, Heidelberg University, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany.
2
Institute of Neuroscience, Fourth Military Medical University, 17 West Chang-le Road, Xi'an 710032, China.
3
Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut 06030-3401, USA.
4
1] Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut 06030-3401, USA [2] Department of Molecular Biology and Biophysics, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut 06030-3401, USA.

Abstract

Synaptic plasticity is the cornerstone of processes underlying persistent nociceptive activity-induced changes in normal nociceptive sensitivity. Kalirin-7 is a multifunctional guanine-nucleotide-exchange factor (GEF) for Rho GTPases that is characterized by its localization at excitatory synapses, interactions with glutamate receptors and its ability to dynamically modulate the neuronal cytoskeleton. Here we show that spinally expressed Kalirin-7 is required for persistent nociceptive activity-dependent synaptic long-term potentiation as well as activity-dependent remodelling of synaptic spines in the spinal dorsal horn, thereby orchestrating functional and structural plasticity during the course of inflammatory pain.

PMID:
25865668
PMCID:
PMC4403379
DOI:
10.1038/ncomms7820
[Indexed for MEDLINE]
Free PMC Article

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