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J Physiol Volume 532, Number 1, 241-250, April 1, 2001
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Journal of Physiology (2001), 532.1, pp. 241-250
© Copyright 2001 The Physiological Society

Functional reorganization of sensory pathways in the rat spinal dorsal horn following peripheral nerve injury


M. Okamoto , H. Baba , P. A. Goldstein †, H. Higashi ‡, K. Shimoji and M. Yoshimura §


§ Department of Physiology, Saga Medical School, Saga 849-8501, ‡ Department of Physiology, Kurume University School of Medicine, Kurume 830-0011, Department of Anaesthesiology, Niigata University, School of Medicine, Niigata 951-8510, Japan and † Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032-3784, USA

  1. Functional reorganization of sensory pathways in the rat spinal dorsal horn following sciatic nerve transection was examined using spinal cord slices with an attached dorsal root. Slices were obtained from animals whose sciatic nerve had been transected 2-4 weeks previously and compared to sham-operated controls.

  2. Whole-cell recordings from substantia gelatinosa neurones in sham-operated rats, to which nociceptive information was preferentially transmitted, revealed that dorsal root stimulation sufficient to activate Adelta afferent fibres evoked a mono- and/or polysynaptic EPSC in 111 of 131 (~85 %) neurones. This is in contrast to the response following Abeta fibre stimulation, where monosynaptic EPSCs were observed in 2 of 131 (~2 %) neurones and polysynaptic EPSCs were observed in 18 of 131 (~14 %) neurones.

  3. In sciatic nerve-transected rats, however, a polysynaptic EPSC following stimulation of Abeta afferents was elicited in 30 of 37 (81 %) neurones and a monosynaptic EPSC evoked by Abeta afferent stimulation was detected in a subset of neurones (4 of 37, ~11 %).

  4. These observations suggest that, following sciatic nerve transection, large myelinated Abeta afferent fibres establish synaptic contact with interneurones and transmit innocuous information to substantia gelatinosa. This functional reorganization of the sensory circuitry may constitute an underlying mechanism, at least in part, for sensory abnormalities following peripheral nerve injuries.




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