Estupina C, Abarca J, Arancibia S, Belmar J
Laboratoire Plasticite et Adaptation Cellulaires, ERS 5644 du CNRS, Université Montpellier 2, France.
Neurosci Lett. 1996 Nov 29;219(3):203-6. doi: 10.1016/s0304-3940(96)13211-0.
The median eminence (ME) push-pull perfusion technique was used in this work and the results clearly showed that i.p. administration of MK-801 (4 mg/kg), a specific N-methyl-D-aspartate (NMDA) receptor antagonist, totally abolished dexamethasone (Dex) (300 micrograms/ 100 g i.p. injected) and immobilization stress-induced hypothalamic somatostatin release in adult male rats. We also observed that glutamate from median eminence-hypothalamic medio basal (ME-MBH) complex, measured by high performance liquid chromatography (HPLC), exhibited a conspicuous secretory pattern, with the total amount released not modified by Dex administration. This indicates that Dex and stress-induced somatostatin (SS) secretion is not mediated by endogenous glutamate variations but likely by activation of NMDA receptors.
本研究采用正中隆起（ME）推挽式灌注技术，结果清楚地表明，腹腔注射特异性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801（4mg/kg）可完全消除成年雄性大鼠腹腔注射地塞米松（Dex，300μg/100g）和制动应激诱导的下丘脑生长抑素释放。我们还观察到，通过高效液相色谱法（HPLC）测定，来自正中隆起-下丘脑中间基底部（ME-MBH）复合体的谷氨酸呈现出明显的分泌模式，其释放总量不受地塞米松给药的影响。这表明地塞米松和应激诱导的生长抑素（SS）分泌不是由内源性谷氨酸变化介导的，而是可能由NMDA受体激活介导的。
