Chakrabarti Nilkanta, Ray Arun K
Department of Physiology, Rammohan College, 102/1-Raja Rammohan Sarani, Calcutta 700 009, India.
Neuroreport. 2003 Aug 6;14(11):1497-501. doi: 10.1097/00001756-200308060-00019.
Triiodothyronine (T3) stimulated AChE activity in depolarization-induced intact synaptosomes (isolated from adult rat cerebral cortex) suspended in calcium-supplemented choline chloride buffer in a time-dependent manner maximally 45-60 s after T3 administration and in a dose-dependent manner with an optimum at 10-100 nM. T3 (100 nM) had no such effects on AChE activity in synaptosomes at non-depolarized conditions. There was no direct effect of T3 on AChE activity of lysed synaptosomal suspension in the physiological range (nM) of T3. The experiments suggest that T3 might have a role in the calcium-dependent release/co-release of acetylcholine from intact synaptosomes concomitant with the acceleration of choline uptake mechanisms that has been reported to accompany elevation of AChE activity. Additionally, electron microscopic structures showed condensation of the cytosolic content with increase in electron density, formation of intrasynaptosomal coarse vesicles and appearance of vesicular fusion like structures (meandering) at the periphery in depolarization-induced T3-treated (60 s) intact synaptosomes, indicating the occurrence of the release of neurotransmitters. The present investigation indicates a definite role of T3 on Ca2+-dependent cholinergic neurotransmission.
三碘甲状腺原氨酸（T3）以时间依赖性方式刺激悬浮于补充钙的氯化胆碱缓冲液中的去极化诱导的完整突触体（从成年大鼠大脑皮层分离）中的乙酰胆碱酯酶（AChE）活性，在给予T3后最大45 - 60秒时达到峰值，且呈剂量依赖性，最佳浓度为10 - 100 nM。T3（100 nM）在非去极化条件下对突触体中的AChE活性无此类影响。在T3的生理范围（nM）内，T3对裂解的突触体悬浮液的AChE活性无直接影响。实验表明，T3可能在完整突触体中乙酰胆碱的钙依赖性释放/共释放中起作用，同时加速胆碱摄取机制，据报道这与AChE活性升高相伴。此外，电子显微镜结构显示，在去极化诱导的T3处理（60秒）的完整突触体中，胞质内容物浓缩，电子密度增加，突触体内出现粗大囊泡，周边出现囊泡融合样结构（蜿蜒状），表明神经递质发生了释放。本研究表明T3在Ca2 +依赖性胆碱能神经传递中具有明确作用。
