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首页> 外文期刊>Brain research >GABAA receptors in the central nucleus of amygdala (CeA) affect on pain modulation.
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GABAA receptors in the central nucleus of amygdala (CeA) affect on pain modulation.

机译：杏仁核中央核中的GABAA受体（CeA）影响疼痛调节。

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The central nucleus of the amygdala (CeA), the nociceptive amygdala, serves as the major output nucleus of the amygdala and participates in receiving and processing pain information. Considering the abundance of GABA(A) receptors in the CeA and also the attributed bidirectional roles for GABA in controlling nociception, we examined the effects of bilateral intra-CeA microinjection of a different dose of the GABA(A) receptor agonist, muscimol, and the GABA(A) receptor antagonist, bicuculline, on pain modulation using a tail-flick test. Adult rats were exposed to intra-CeA microinjection of a selective GABA(A) receptor antagonist, bicuculline, (50,100,200,400 ng/side) or a selective GABA(A) receptor agonist, muscimol, (62.5, 125,250,500 ng/side) and subjected to the tail-flick test. Tail-flick latencies were measured every 5 min after drug microinjection for 60 min. Microinjection of bicuculline and muscimol into the CeA increased and decreased tail-flick latency, respectively in a dose-dependent fashion. The hyperalgesic effect of muscimol (500 ng) microinjected into the CeA was attenuated (P<0.001) by a prior microinjection of bicuculline (50 ng) at the same site. The results of the present study showed that locally released GABA in the CeA is involved in pain modulation and suggests the existence of a GABA(A) mediated inhibitory system in the CeA on pain control.
机译：杏仁核（CeA）的中央核（伤害性杏仁核）是杏仁核的主要输出核，并参与接收和处理疼痛信息。考虑到CeA中GABA（A）受体的丰富性以及归因于GABA在控制伤害感受中的双向作用，我们研究了不同剂量的GABA（A）受体激动剂，麝香酚和双剂量的双侧CeA显微注射的作用。使用甩尾试验调节疼痛的GABA（A）受体拮抗剂bicuculline成年大鼠接受选择性GABA（A）受体拮抗剂，双小分子（50,100,200,400 ng /侧）或选择性GABA（A）受体激动剂，麝香酚（62.5、125,250,500 ng /侧）的CeA显微注射，并接受甩尾测试。药物显微注射60分钟后，每5分钟测量一次甩尾潜伏期。将双小分子和麝香酚微注射到CeA中，分别以剂量依赖性方式增加和减少了甩尾潜伏期。事先在同一部位双胆碱（50 ng）显微注射，将微注射到CeA中的麝香酚（500 ng）的镇痛作用减弱（P <0.001）。本研究的结果表明，在CeA中局部释放的GABA参与了疼痛调节，并表明在CeA中存在GABA（A）介导的抑制疼痛的抑制系统。

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