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J Neurophysiol 92: 1417-1432, 2004. First published April 21, 2004; doi:10.1152/jn.00874.2003
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Location and Magnitude of Conductance Changes Produced by Renshaw Recurrent Inhibition in Spinal Motoneurons

Mitchell G. Maltenfort, Martha L. McCurdy, Carrie A. Phillips, Vladimir V. Turkin and Thomas M. Hamm

Division of Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona 85013

Submitted 8 September 2003; accepted in final form 13 April 2004

The mean location of Renshaw synapses on spinal motoneurons and their synaptic conductance were estimated from changes in impedance magnitude produced by sustained recurrent inhibition. Motoneuron impedance was determined by injecting quasi-white noise current into lumbosacral motoneurons of pentobarbital-anesthetized cats. Synaptic location and conductance were estimated by comparing observed impedance changes to simulation results obtained using standard motoneuron models and compartmental models fit to each impedance function. Estimated synaptic locations ranged from 0.10 to 0.41{lambda}, with a mean of 0.19 or 0.24{lambda}, depending on the estimation method. Average dendritic path length was 262 µm. Average synaptic conductance was 23 to 27 nS (range: 6.7 to 57.9 nS), corresponding to conductance changes of 78 to 88% of resting membrane conductance. Estimated accuracy was supported by consistency using different estimation methods, agreement with Fyffe's 1991 morphological data, and comparisons of observed and simulated recurrent IPSP amplitudes. Synaptic location, but not synaptic conductance, was correlated with rheobase, a measure of motoneuron excitability. Synaptic conductance did not depend on synaptic location. A regression analysis demonstrated that synaptic conductance and cell impedance were the principal factors determining recurrent IPSP amplitude. Simulations using the observed values and locations of Renshaw conductance demonstrate that recurrent inhibition can require as much as an additional 14 to 18% sustained excitatory synaptic conductance to depolarize motoneurons sufficiently to activate somatic or dendritic inward currents and recruit motoneurons or amplify excitatory synaptic currents.


Address for reprint requests and other correspondence: T. M. Hamm, Division of Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, 350 W. Thomas Rd., Phoenix, AZ 85013 (E-mail: thamm{at}chw.edu).




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