Arem R, Chayoth R, Shenkenberg T D, Miller S I, Chou M C, Field J B
Arch Biochem Biophys. 1983 Aug;225(1):66-74. doi: 10.1016/0003-9861(83)90007-3.
An initial incubation of dog thyroid slices with 0.1 or 1 microM acetylcholine (ACH) for at least 2 h decreases its subsequent stimulation of [1-14C]glucose oxidation. Refractoriness persists for as long as 6 h in the absence of ACH. While new protein synthesis is essential for recovery, it is not necessary for its induction. Refractoriness is prevented when 25 microM tropicamide, an atropine-like drug, is present from the beginning of the initial incubation, but not when it is added after 2 h of incubation of slices with ACH, indicating that at this time ACH is no longer necessary for refractoriness. During refractoriness induced by ACH, stimulation of glucose oxidation by thyroid-stimulating hormone, prostaglandin E1, dibutyryl cyclic AMP, and cholera toxin, but not menadiol, is also significantly diminished. Incubation of thyroid slices with ACH does not modify its stimulation of iodide organification or 32Pi incorporation into phospholipids. These results suggest that the desensitization is not due to changes in the ACH receptor but rather to intracellular metabolic effects. This phenomenon may be important in the regulation of cholinergic effects on the thyroid.
将犬甲状腺切片先用0.1或1微摩尔乙酰胆碱（ACH）孵育至少2小时，会降低其随后对[1-¹⁴C]葡萄糖氧化的刺激作用。在无ACH的情况下，不应性可持续长达6小时。虽然新蛋白质合成对于恢复至关重要，但对于不应性的诱导并非必需。若在最初孵育开始时就加入25微摩尔托吡卡胺（一种类似阿托品的药物），则可防止不应性的发生，但在甲状腺切片与ACH孵育2小时后再添加该药物则无效，这表明此时ACH对于不应性已不再必要。在由ACH诱导的不应性期间，促甲状腺激素、前列腺素E1、二丁酰环磷腺苷和霍乱毒素对葡萄糖氧化的刺激作用也显著减弱，但维生素K₄的刺激作用未受影响。用ACH孵育甲状腺切片不会改变其对碘有机化或³²Pi掺入磷脂的刺激作用。这些结果表明，脱敏作用并非由于ACH受体的变化，而是由于细胞内代谢效应。这种现象可能在胆碱能对甲状腺的作用调节中具有重要意义。
