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Effect of Electrical Field Stimulation on Dorsal Root Ganglion Neuronal Function

Authors


  • Conflict of Interest: Quinn H. Hogan, MD, has received fees for serving as a consultant for Spinal Modulation, Inc. and has received research funding from Spinal Modulation, Inc. Jeffrey Kramer, PhD, is an employee of Spinal Modulation, Inc. The other authors reported no conflicts of interest.
  • For more information on author guidelines, an explanation of our peer review process, and conflict of interest informed consent policies, please go to http://www.wiley.com/bw/submit.asp?ref=1094-7159&site=1
  • Source(s) of financial support: Funds were provided by a grant from Spinal Modulation, Inc.

Address correspondence to: Quinn H. Hogan, MD, Medical College of Wisconsin, 8701 W Watertown Plank, Milwaukee, WI 53226-3548, USA. Email: qhogan@mcw.edu

Abstract

Objectives

Neural stimulation may provide analgesia for a variety of painful conditions. Activation of primary sensory neurons, which underlies pain relief by spinal cord stimulation, also may be achieved by stimulation at the level of the dorsal root ganglion (DRG). The DRG also is a site of pain pathogenesis, particularly in neuropathic pain. We therefore examined the hypothesis that field stimulation of the DRG directly suppresses excitability of sensory neurons.

Materials and Methods

Intercellular Ca2+ level (Fura-2 microfluorimetry) and membrane potential were recorded in excised rat DRGs with ganglionic field stimulation (GFS) delivered by wire electrodes in the bath solution adjacent to the DRG. Neuronal excitability was evaluated by number of action potentials (APs) generated during neuronal depolarization, conduction velocity during axonal stimulation, and AP propagation failure. These were measured before and after 90 sec of GFS at 60 Hz. Data analysis employed chi-square, paired t-test, and analysis of variance.

Results

GFS using 400-μsec pulses and 30 V generated Ca2+ influx, indicative of DRG neuronal activation. Fewer neurons were able to fire one or more APs after GFS (N = 23) than in control neurons without GFS (N = 24, p < 0.05), and fewer neurons were able to generate multiple APs after GFS compared with time controls (p < 0.05). GFS significantly reduced conduction velocity compared with baseline before GFS (N = 16, p < 0.05) while there was no change in the controls (N = 18). The peak rate at which APs could be propagated was reduced in 9 of 16 neurons by GFS, but propagation efficiency was reduced in only 4 of 18 control neurons (p < 0.05), and the total number of APs generated in an ensemble of stimuli at different frequencies was reduced by GFS (N = 16, p < 0.05) but not in time controls (N = 18).

Conclusions

Our findings indicate that direct excitation of the DRG by electrical fields reduces neuronal excitability and may provide a new analgesic approach.

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