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Hanna Wootz, Eileen FitzSimons-Kantamneni, Martin Larhammar, Travis M. Rotterman, Anders Enjin, Kalicharan Patra, Elodie André, Brigitte Van Zundert, Klas Kullander and Francisco J. Alvarez Alterations in the motor neuron–renshaw cell circuit in the Sod1G93A mouse model Journal of Comparative Neurology 521

Version of Record online: 18 MAR 2013 | DOI: 10.1002/cne.23266

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In amyotrophic lateral sclerosis, motor neurons are hyperexcitable. Normally, motor neuron firing is controlled by a recurrent feedback inhibitory circuit mediated by Renshaw cells. Analyses in SOD1 mice demonstrate downregulation of postsynaptic nicotinic receptors (Chrna2) and presynaptic VAChT and disassembly of motor axon synapses on calbindin-IR Renshaw cells just before onset of motor symptoms. In contrast, Renshaw cell synapses undergo transitory compensatory sprouting. We conclude that a deficit in feedback inhibition may exacerbate motor neuron excitability and contribute to the disease.

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