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First published online on February 7, 2003.
 Copyright © 2003 by The Physiological Society
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Received November 21, 2002
Accepted after revision January 15, 2003

Peripheral nerve injury in the rat alters excitatory synaptic transmission in lamina II of the dorsal horn

T. Kohno1*, Kimberly A. Moore2, Hiroshi Baba2, and Clifford J. Woolf2

1 Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown MA 02129, USA
2 Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA

* To whom correspondence should be addressed. E-mail: tkohno{at}partners.org.

Using the blind whole cell patch-clamp recording technique, we investigated peripheral nerve injury-induced changes in excitatory synaptic transmission to neurones in lamina II of the dorsal horn. Partial (i.e. chronic constriction injury (CCI) and spared nerve injury (SNI)) and complete (i.e. sciatic nerve transection (SNT)) peripheral nerve injury altered the mean threshold intensity for eliciting A fibre-mediated EPSCs in lamina II neurones. Following SNT and CCI, EPSC threshold was significantly decreased, but following SNI, EPSC threshold was increased (naive: 32 ± 2 µA, SNT: 22 ± 2 µA, CCI: 23 ± 2 µA, SNI: 49 ± 4 µA; P < 0.01, Student's unpaired t-test). Despite this disparity between models, dorsal root compound action-potential recordings revealed no significant difference in the conduction velocity or activation threshold of A{beta} and A{delta} fibres in naive, SNT, CCI and SNI rats. In addition to the changes in EPSC threshold, we also observed a shift in the distribution of EPSCs. In spinal cord slices from naive rats, polysynaptic A{beta} fibre-evoked EPSCs were observed in 24 % of lamina II neurones, monosynaptic A{delta} fibre EPSCs were observed in 34 % and polysynaptic A{delta} fibre EPSCs were observed in 7 %. Following SNT and CCI, the percentage of neurones with polysynaptic A{beta} fibre EPSCs increased to >= 65 % of the sampled population, while the percentage of neurones with monosynaptic A{delta} fibre EPSCs decreased to < 10 %. The percentage of neurones with polysynaptic A{delta} fibre EPSCs was unchanged. In contrast, following SNI, A{beta} fibre EPSCs decreased in incidence while the percentage of neurones with polysynaptic A{delta} fibre EPSCs increased to 44 %. Similar to the other injury models, however, monosynaptic A{delta} fibre EPSCs decreased in frequency following SNI. Thus, excitatory synaptic transmission is subject to divergent plasticity in different peripheral nerve injury models, reflecting the complexity of responses to different forms of deafferentation.




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