Role of calcium in acetylcholine-induced desensitization in dog thyroid slices.
Role of calcium in acetylcholine-induced desensitization in dog thyroid slices.
复制标题
钙在乙酰胆碱诱导的狗甲状腺切片脱敏中的作用。
DOI：
10.1016/0003-9861(84)90098-5
复制
发表时间：
1984
影响因子：
3.9
通讯作者：
Field,JB
中科院分区：
文献类型：
--
作者：
Arem,R;Chayoth,R;Shenkenberg,T;Field,JB
1 μ马乙基胆碱（ACH）在狗甲状腺片中孵育3小时，然后在不含ACH的情况下孵育2小时，在第三次孵育45分钟时，ACH对葡萄糖氧化的刺激减弱。在所有培养过程中使用无钙培养基可防止脱敏并减少（但不能消除）乙酰胆碱对葡萄糖氧化的刺激。EGTA[乙二醇双（β-氨基乙醚）-N,N ' -四乙酸]（2mm）添加到所有培养的无钙培养基中，可以防止乙酰胆碱引起的难熔性和葡萄糖氧化刺激。仅在第一次孵育期间，通过使用EGTA和无钙培养基来实现钙的消耗，也可以防止顽固性，但不能增强乙酰胆碱引起的葡萄糖氧化。在第一次孵育3 h时，1 μ μ μ载体A23817对甲状腺切片的葡萄糖氧化刺激减弱，第3次孵育时首次加入1 μ μ马赫的A23817对葡萄糖氧化的刺激减弱。离子载体诱导的脱敏与胆碱能毒蕈碱受体效应无关。1 μmACH初始孵育犬甲状腺片，可减少随后0.5 μ μ微粒对葡萄糖氧化的刺激。然而，ach诱导的对电离层的脱敏可以通过在第三次孵育中增加10倍的电离层量来克服。在第一次孵育中，离子载体（1 μm）对促甲状腺激素（TSH） （10 mU/ml）刺激的葡萄糖氧化也具有抗性。与此相反，甲状腺切片经TSH （25 mU/ml）初始孵育后，第三次孵育时添加0.5 μ μ微孔对葡萄糖氧化的刺激作用不受影响。这些结果表明，细胞内钙的增加在ach诱导的甲状腺脱敏中起主要作用，甚至介导。
Incubation of dog thyroid slices with 1 μmacetylcholine (ACH) for 3 h followed by a second 2-h incubation without it induces a diminution of stimulation of glucose oxidation by ACH during a third incubation of 45 min. Using a calcium-free medium during all incubations prevents the desensitization and reduces, but does not abolish, ACH stimulation of glucose oxidation. EGTA [ethylene glycol bis(β-aminoethyl ether)-N,N′-tetraacetic acid] (2 mm) added to the calcium-free medium in all incubations prevents both refractoriness and stimulation of glucose oxidation induced by ACH. Calcium depletion during the first incubation only, achieved by using EGTA and a calcium-free medium, also prevents refractoriness but not the augmentation of glucose oxidation caused by ACH. Incubation of thyroid slices with 1 μmionophore A23817 during the 3-h first incubation decreases the stimulation of glucose oxidation induced by its readdition or by 1 μmACH added for the first time in the third incubation. Ionophore-induced desensitization is not related to a cholinergic muscarinic receptor effect. Initial incubation of dog thyroid slices with 1 μmACH diminishes the subsequent stimulation of glucose oxidation by 0.5 μmionophore. However, the ACH-induced desensitization to ionophore can be overcome by a 10-fold increase in the amount of ionophore in the third incubation. Ionophore (1 μm) in the first incubation also induces refractoriness to thyroid-stimulating hormone (TSH) (10 mU/ml)-stimulated glucose oxidation in the third incubation. In contrast, initial incubation of thyroid slices with TSH (25 mU/ml) does not affect the stimulation of glucose oxidation by 0.5 μmionophore added during the third incubation. These results suggest that increased intracellular calcium plays a major role in, or even mediates, ACH-induced desensitization in the thyroid gland.