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Electrical stimulation accelerates and increases expression of BDNF and trkB mRNA in regenerating rat femoral motoneurons

Authors

  • Abdulhakeem A. Al-Majed,

    1. 1 Department of Pharmacology, Division of Neuroscience, 513 Heritage Medical Research Center, University of Alberta, Edmonton, Alberta T6G 2S2, Canada 2 Departments of Orthopaedic Surgery and Neurology, Johns Hopkins Medical School, Baltimore, MD, USA
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  • 1 Thomas M. Brushart,

    1. 1 Department of Pharmacology, Division of Neuroscience, 513 Heritage Medical Research Center, University of Alberta, Edmonton, Alberta T6G 2S2, Canada 2 Departments of Orthopaedic Surgery and Neurology, Johns Hopkins Medical School, Baltimore, MD, USA
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  • and 2 Tessa Gordon 1

    1. 1 Department of Pharmacology, Division of Neuroscience, 513 Heritage Medical Research Center, University of Alberta, Edmonton, Alberta T6G 2S2, Canada 2 Departments of Orthopaedic Surgery and Neurology, Johns Hopkins Medical School, Baltimore, MD, USA
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: Dr Tessa Gordon, as above.
E-mail: tessa.gordon@ualberta.ca

Abstract

Electrical stimulation promotes the speed and accuracy of motor axonal regeneration. The positive effects of stimulation are mediated at the cell body. Here we characterize the effect of electrical stimulation on motoneuronal expression of BDNF and its receptor, trkB, two genes whose expression levels in motoneurons correlate with regeneration and are regulated by electrical activity in a variety of neurons. We used semiquantitative in situ hybridization to measure expression of mRNA encoding BDNF and the full-length trkB receptor at intervals of 8 h, 2 days and 7 days after unilateral femoral nerve cut, suture, and stimulation. Expression in regenerating motoneurons was compared to that of contralateral intact motoneurons. BDNF and trkB signals were not significantly upregulated 8 h and 2 days after femoral nerve suture and sham stimulation. By 7 days, there was a 2-fold increase in both BDNF and trkB mRNA expression. In contrast, stimulation of cut and repaired nerves for only 1 h led to rapid upregulation of BDNF and trkB mRNA by 3-fold and 2-fold, respectively, within the first 8 h. The stimulation effect peaked at 2 days with 6-fold and 4-fold increases in the signals, respectively. Thereafter, the levels of BDNF and trkB mRNA expression declined to equal the 2-fold increase seen at 7 days after nerve repair and sham-stimulation. We conclude that brief electrical stimulation stimulates BDNF and trkB expression in regenerating motoneurons. Because electrical stimulation is known to accelerate axonal regeneration, we suggest that changes in the expression of BDNF and trkB correlate with acceleration of axonal regeneration.

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