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 muA, SNT: 22 +/-2 muA, CCL 23 +/- 2 muA, SNI: 49 +/- 4 muA; P < 0.01, Student's impaired 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 and Ad 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 fibre-evoked EPSCs were observed in 24 % of lamina II neurones, monosynaptic Ad fibre EPSCs were observed in 34 % and polysynaptic Ad fibre EPSCs were observed in 7 %. Following SNT and CCI, the percentage of neurones with polysynaptic Adelta fibre EPSCs increased to greater than or equal to 65 % of the sampled population, while the percentage of neurones with monosynaptic Adelta fibre EPSCs decreased to < 10 %. The percentage of neurones with polysynaptic Ad fibre EPSCs was unchanged. In contrast, following SNI, Abeta fibre EPSCs decreased in incidence while the percentage of neurones with polysynaptic Adelta fibre EPSCs increased to 44 %. Similar to the other injury models, however, monosynaptic Ad 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.