Department of General Surgery, Xijing Hospital; The Fourth Military Medical University, Xi'an 710032, China.
Mol Pain. 2014 Jun 18;10:38. doi: 10.1186/1744-8069-10-38.
Thyroid hormones are essential for the maturation and functions of the central nervous system. Pain sensitivity is related to the thyroid status. However, information on how thyroid hormones affect pain processing and synaptic transmission in the anterior cingulate cortex (ACC) is limited. Nociceptive threshold and synaptic transmission in the ACC were detected in the experimental hypothyroidism (HT) mice.
HT was induced by methimazole and potassium perchlorate in distilled drinking water for 4 weeks. The threshold of pain perception to hot insults, but not mechanical ones, decreased in hypothyroid mice. After treatment with tri-iodothyronine (T3) or thyroxine (T4) for 2 weeks, thermal pain threshold recovered. Electrophysiological recordings revealed enhanced glutamatergic synaptic transmission and reduced GABAergic synaptic transmission in the ACC. Supplementation with T3 or T4 significantly rescued this synaptic transmission imbalance. In the same model, HT caused the up-regulation of the GluR1 subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor and NR2B-containing N-methyl-D-aspartate receptors, but it down-regulated γ-aminobutyric acid A receptors in the ACC. Supplementation with T3 or T4 notably recovered the levels of above proteins.
These results suggest that HT promotes hypersensitivity to noxious thermal, and that supplementation with T3 or T4 rescues the imbalance between excitatory and inhibitory transmission in the ACC.
甲状腺激素对中枢神经系统的成熟和功能至关重要。疼痛敏感性与甲状腺状态有关。然而，关于甲状腺激素如何影响前扣带皮层（ACC）中的疼痛处理和突触传递的信息有限。在实验性甲状腺功能减退症（HT）小鼠中检测到 ACC 的痛觉阈值和突触传递。
在 4 周的时间里，用甲巯咪唑和高氯酸钾在蒸馏饮用水中诱导 HT。甲状腺功能减退小鼠对热刺激的疼痛感知阈值降低，但对机械刺激的疼痛感知阈值没有降低。用三碘甲状腺原氨酸（T3）或甲状腺素（T4）治疗 2 周后，热痛阈值恢复。电生理记录显示 ACC 中的谷氨酸能突触传递增强，γ-氨基丁酸能突触传递减弱。补充 T3 或 T4 可显著纠正这种突触传递失衡。在相同模型中，HT 导致 α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体的 GluR1 亚基和含有 NR2B 的 N-甲基-D-天冬氨酸受体上调，但下调 ACC 中的γ-氨基丁酸 A 受体。补充 T3 或 T4 可显著恢复上述蛋白的水平。
这些结果表明 HT 促进了对有害热刺激的过敏反应，补充 T3 或 T4 可挽救 ACC 中兴奋性和抑制性传递之间的失衡。
