GABA and
glycine are inhibitory
neurotransmitters used by many neurons in the spinal dorsal horn, and intrathecal administration of
GABA(A) and
glycine receptor antagonists produces behavioural signs of
allodynia, suggesting that these transmitters have an important role in spinal
pain mechanisms. Several studies have described a substantial loss of
GABA-immunoreactive neurons from the dorsal horn in nerve injury models, and it has been suggested that this may be associated with a loss of inhibition, which contributes to the behavioural signs of
neuropathic pain. We have carried out a quantitative stereological analysis of the proportions of neurons in laminae I, II and III of the rat dorsal horn that show
GABA- and/or
glycine-immunoreactivity 2 weeks after nerve
ligation in the chronic constriction injury (CCI) model, as well as in
sham-operated and nai;ve animals. At this time, rats that had undergone CCI showed a significant reduction in the latency of withdrawal of the ipsilateral hindpaw to a radiant heat stimulus, suggesting that
thermal hyperalgesia had developed. However, we did not observe any change in the proportion of neurons in laminae I-III of the ipsilateral dorsal horn that showed
GABA- or
glycine-immunoreactivity compared to the contralateral side in these animals, and these proportions did not differ significantly from those seen in
sham-operated or nai;ve animals. In addition, we did not see any evidence for alterations of
GABA- or
glycine-immunostaining in the neuropil of laminae I-III in the animals that had undergone CCI. Our results suggest that significant loss of GABAergic or glycinergic neurons is not necessary for the development of
thermal hyperalgesia in the CCI model of
neuropathic pain.