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Chemical communication between regenerating motor axons and Schwann cells in the growth pathway

Authors

  • Gerta Vrbova,

    1. Autonomic Neuroscience Centre, Royal Free and University College Medical School, London, UK
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  • Neeraj Mehra,

    1. Division of Physical Medicine and Rehabilitation/Centre for Neuroscience, 525 Heritage Medical Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada T6G 2S2
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  • Harei Shanmuganathan,

    1. Division of Physical Medicine and Rehabilitation/Centre for Neuroscience, 525 Heritage Medical Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada T6G 2S2
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  • Neil Tyreman,

    1. Division of Physical Medicine and Rehabilitation/Centre for Neuroscience, 525 Heritage Medical Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada T6G 2S2
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  • Melitta Schachner,

    1. Zentrum für Molekulare Neurobiologie, Universität Hamburg, Germany and Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA
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  • Tessa Gordon

    1. Division of Physical Medicine and Rehabilitation/Centre for Neuroscience, 525 Heritage Medical Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada T6G 2S2
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Dr Tessa Gordon, as above.
E-mail: tessa.gordon@ualberta.ca

Abstract

There are receptors on denervated Schwann cells that may respond to the neurotransmitters that are released from growth cones of regenerating motor axons. In order to ascertain whether the interaction of the transmitters and their receptors plays a role during axon regeneration, we investigated whether pharmacological block of the interaction would reduce the number of motoneurons that regenerate their axons after nerve section and surgical repair. Peripheral nerves in the hindlimbs of rats and mice were cut and repaired, and various drugs were applied to the peripheral nerve stump either directly or via mini-osmotic pumps over a 2–4-week period to block the binding of acetylcholine to nicotinic and muscarinic acetylcholine receptors (AChRs: α-bungarotoxin, tubocurarine, atropine and, gallamine) and binding of ATP to P2Y receptors (suramin). In rats, the nicotinic AChR antagonistic drugs and suramin reduced the number of motoneurons that regenerated their axons through the distal nerve stump. In mice, suramin significantly reduced the upregulation of the carbohydrate HNK-1 on the Schwann cells in the distal nerve stump that normally occurs during motor axon regeneration. These data indicate that chemical communication between regenerating axons and Schwann cells during axon regeneration via released neurotransmitters and their receptors may play an important role in axon regeneration.

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