Responses of Dorsal Column Nuclei Neurons in Rats with Experimental Mononeuropathy

To examine the functional role of dorsal column nuclei in neuropathic pain, electrophysiological properties of low- and high-threshold dorsal column nuclei neurons in neuropathic and normal rats were examined. Single-neuronal activities were recorded from the gracile nucleus (GN) in rats at 10-14 days after application of four loose ligatures around the sciatic nerve (chronic constriction nerve injury; CCI). A total of 190 units were recorded from the GN in naive and CCI rats. The largest population of low-threshold mechanoreceptive (LTM) neurons recorded from the GN of naive rats were classified as rapidly-adapting (RA) LTM neurons, whereas those from CCI rats were slowly-adapting (SA) neurons. Mean orthodromic latencies of GN neurons ipsilateral to the CCI after sciatic nerve stimulation were significantly longer than those of naive animals and those of GN neurons without receptive fields were significantly longer than any other type of neurons. One hundred and eight of 190 GN neurons were also antidromically activated following electrical stimulation of the ventro-lateral posterior nucleus of the thalamus. Furthermore, when stronger stimuli were applied to the sciatic nerve, some GN neurons also responded with long latencies. GN neurons of sham-operated naive rats and those contralateral to the CCI had mechanical receptive fields on the paw, whereas 8.0% of the GN neurons in the CCI side did not have any detectable mechanical receptive field. Receptive field size was not significantly different between neurons ipsilateral or contralateral to the CCI and those of naive rats. Spontaneous activity of GN neurons from the ipsilateral side was significantly higher than those from the contralateral side. On the other hand, spontaneous activity of GN neurons both ipsilateral and contralateral to the CCI were significantly higher than those from naive rats. Furthermore, afterdischarges of GN neurons ipsilateral and contralateral to the CCI were significantly higher than those of naive rats. The present data suggest that the dorsal column pathway is involved in CCI-produced sensory abnormalities by conveying their hyperactivity to thalamic neurons.