Pharmacological inactivation of the primate posterior insular/secondary somatosensory cortices attenuates thermal hyperalgesia
Pharmacological inactivation of the primate posterior insular/secondary somatosensory cortices attenuates thermal hyperalgesia
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DOI：
10.1002/ejp.1996
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发表时间：
2022-06
影响因子：
3.6
通讯作者：
K. Nagasaka;I. Takashima;K. Matsuda;N. Higo
中科院分区：
文献类型：
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作者：
K. Nagasaka;I. Takashima;K. Matsuda;N. Higo
我们之前建立了一个中枢性卒中后疼痛（CPSP）的猕猴模型，并通过结合成像技术和局部药物失活证实了后岛叶皮层（PIC）和次级体感皮层（SII）对机械性异常性疼痛中体感刺激的活动增加。然而，目前还不清楚同样的干预是否对热痛觉过敏有效。因此，使用猕猴模型，我们研究了药理学失活后的PIC/SII的热刺激的行为反应。
We previously established a macaque model of central post‐stroke pain (CPSP) and confirmed the involvement of increased activity of the posterior insular cortex (PIC) and secondary somatosensory cortex (SII) to somatosensory stimuli in mechanical allodynia by a combination of imaging techniques with local pharmacological inactivation. However, it is unclear whether the same intervention would be effective for thermal hyperalgesia. Therefore, using the macaque model, we examined behavioural responses to thermal stimuli following pharmacological inactivation of the PIC/SII.