Neuropathic pain is defined as the pain that results from functional abnormalities of the nervous system: for example, deafferentiation or dysesthesia, referring to an unfamiliar unpleasant sensation, persisting for a long duration even in the absence of ongoing active tissue-damaging process to explain it. Although peripheral neural mechanisms are likely to contribute, in part, to the neuropathic pain, the persistence of pain after healing of the damaged tissue suggests that plastic changes in the CNS, including the spinal cord, may also play an important role in processing the transmission of neuropathic pain. Present study was designed to investigate the plastic change in synaptic transmission at the spinal level using whole cell patch clamp recordings from substantia gelatinosa (SG, lamina II of Rexed) neurons in spinal cord slices which retained an attached dorsal root dissected from adult rats with or without sciatic nerve transection (SNT). The normal and SNT rats showed no significant differences in passive and active membrane characteristics, including membrane potential, input resistance and configuration of action potential and spike after potentials. In the control rats, primary afferent stimuli with intensity sufficient to activate Aδ afferents elicited a monosynaptic fast excitatory postsynaptic current (EPSC) in 50% of neurons and a polysynaptic EPSC in 30%. In only 5% of neurons, the polysynaptic EPSC was elicited with intensity sufficient to activate Aβ afferents. In the SNT rats, however, a polysynaptic EPSC with a long latency was evoked in 79% of neurons by activation of Aβ afferents.
Increasing stimulus intensity sufficient to activate Aδ afferents produced a EPSC which had a short and constant latency, suggesting that the Aδ afferents were functionally preserved after peripheral nerve transection. Aβ afferent-evoked monosynaptic EPSC was observed in only 2 of 34 neurons. The conduction velocity and minimum stimulus intensity for activation of Aβ and Aδ afferent fibers, assessed by intracellular recordings from dorsal root ganglion neurons, were not significantly altered in normal and sciatic nerve transected rats. These observations suggest that synaptic plasticity may occur in a subset of dorsal horn neurons and/or terminal arborization of primary afferent, particularly Aβ afferents, following nerve transection, consequently sensory information conveyed by Aβ afferents is transmitted to SG neurons which receive a few Aβ afferent inputs in the normal condition. This plastic changes in synaptic organization in the spinal dorsal horn may, therefore, underlie in part pathological pain such as allodynia and dysesthesia.
