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Neuron. 2014 Jan 8;81(1):120-9. doi: 10.1016/j.neuron.2013.10.060.

Neuronal Ig/Caspr recognition promotes the formation of axoaxonic synapses in mouse spinal cord.

Author information

1
Neuroscience Program, Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA; Developmental Biology Program, Sloan-Kettering Institute, New York, NY 10065, USA.
2
Howard Hughes Medical Institute, Kavli Institute of Brain Science, Departments of Neuroscience, Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA.
3
Neuroscience Program, Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA; Developmental Biology Program, Sloan-Kettering Institute, New York, NY 10065, USA; Weill Cornell/Rockefeller/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY 10065, USA.
4
Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel.
5
Department of Bioengineering, Nagaoka University of Technology, 1603-1, Kamitomiokamachi, Nagaoka, Niigata 940-2188, Japan.
6
Department of Bioengineering, Nagaoka University of Technology, 1603-1, Kamitomiokamachi, Nagaoka, Niigata 940-2188, Japan; Nagaoka National College of Technology, 888, Nishikatakaimachi, Nagaoka, Niigata 940-8532, Japan.
7
Howard Hughes Medical Institute, Kavli Institute of Brain Science, Departments of Neuroscience, Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA. Electronic address: tmj1@columbia.edu.
8
Neuroscience Program, Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA; Developmental Biology Program, Sloan-Kettering Institute, New York, NY 10065, USA. Electronic address: kaltschj@mskcc.org.

Abstract

Inhibitory microcircuits are wired with a precision that underlies their complex regulatory roles in neural information processing. In the spinal cord, one specialized class of GABAergic interneurons (GABApre) mediates presynaptic inhibitory control of sensory-motor synapses. The synaptic targeting of these GABAergic neurons exhibits an absolute dependence on proprioceptive sensory terminals, yet the molecular underpinnings of this specialized axoaxonic organization remain unclear. Here, we show that sensory expression of an NB2 (Contactin5)/Caspr4 coreceptor complex, together with spinal interneuron expression of NrCAM/CHL1, directs the high-density accumulation of GABAergic boutons on sensory terminals. Moreover, genetic elimination of NB2 results in a disproportionate stripping of inhibitory boutons from high-density GABApre-sensory synapses, suggesting that the preterminal axons of GABApre neurons compete for access to individual sensory terminals. Our findings define a recognition complex that contributes to the assembly and organization of a specialized GABAergic microcircuit.

PMID:
24411736
PMCID:
PMC3898991
DOI:
10.1016/j.neuron.2013.10.060
[Indexed for MEDLINE]
Free PMC Article

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