Peripheral nerve injury alters excitatory synaptic transmission in lamina II of the rat dorsal horn.
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 mu A, SNT: 22 +/- 2 mu A, CCI: 23 +/- 2 mu A, SNI: 49 +/- 4 mu A; 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 > or = 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.
Kohno
Tatsuro
T
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA. tkohno@partners.org
Moore
Kimberly A
KA
Baba
Hiroshi
H
Woolf
Clifford J
CJ
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D003251:Constriction, Pathologic / Q000473:pathology; D004594:Electrophysiology; D018846:Excitatory Amino Acids / Q000502:physiology*; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology; D018408:Patch-Clamp Techniques; D059348:Peripheral Nerve Injuries; D020671:Posterior Horn Cells / Q000502:physiology*; D051381:Rats; D012584:Sciatic Nerve / Q000293:injuries; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*
D018846:Excitatory Amino Acids