神经病理性疼痛
脊髓
痛觉过敏
甘氨酸受体
痛觉超敏
神经油
医学
神经损伤
麻醉
伤害
加巴能
神经科学
抑制性突触后电位
化学
甘氨酸
内分泌学
中枢神经系统
内科学
受体
生物
生物化学
氨基酸
作者
Erika Polgár,David I. Hughes,John S. Riddell,David Maxwell,Zita Puskár,Andrew J. Todd
出处
期刊:Pain
[Ovid Technologies (Wolters Kluwer)]
日期:2003-07-01
卷期号:104 (1): 229-239
被引量:217
标识
DOI:10.1016/s0304-3959(03)00011-3
摘要
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.
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