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EFFECTS OF INHALATION ANESTHETICS ON KAINATE-INDUCED GLUTAMATE RELEASE FROM CEREBELLAR GRANULE CELLS

机译:吸入麻醉药对海藻酸盐诱导的小脑颗粒细胞谷氨酸释放的影响

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The mechanisms of inhalation anesthesia may include inhibiting non-NMDA excitatory amino acid neurotransmission. This possibility was addressed by measuring the effect of three anesthetics at clinically relevant concentrations on kainate-induced glutamate release from cerebellar granule cells. Cerebellar granule cells were obtained from 8-day-old SD rats and maintained in vitro for 9-14 days. Medium glutamate concentrations were measured by HPLC after 90 minutes incubation with kainate or NMDA. Inhalation anesthetics were introduced by holding the cells under a continuous flow of air/anesthetic mixtures. All anesthetics tested did not effect NMDA-induced glutamate release. Halothane (1 MAC), isoflurane (1 MAC) inhibited kainate-induced glutamate release from the cultured cells whereas enflurane (1 MAC) had no effect on kainate-induced glutamate release. The difference between:enflurane and the other anesthetics tested suggests that anesthesia is dependent on more than one process and the extent at which each function is perturbed is dependent on the specific anesthetic used. Halothane inhibition of kainate-induced glutamate release was not reversible by increasing kainate concentration, indicating halothane does not directly compete with kainate at its receptor. [References: 41]
机译:吸入麻醉的机制可能包括抑制非NMDA兴奋性氨基酸神经传递。通过在临床相关浓度下测量三种麻醉剂对海藻酸盐诱导的谷氨酸从小脑颗粒细胞释放的作用来解决这种可能性。从8日龄SD大鼠获得小脑颗粒细胞,并在体外维持9-14天。与海藻酸盐或NMDA孵育90分钟后,通过HPLC测量中等谷氨酸浓度。通过将细胞保持在连续的空气/麻醉混合物流中来引入吸入麻醉剂。测试的所有麻醉剂均不影响NMDA诱导的谷氨酸释放。氟烷(1 MAC),异氟烷(1 MAC)抑制了海藻酸盐诱导的谷氨酸从培养细胞中的释放,而恩氟烷(1 MAC)对海藻酸盐诱导的谷氨酸的释放没有影响。恩氟烷与其他麻醉药之间的差异表明,麻醉取决于一个以上的过程,每种功能的受扰程度取决于所使用的特定麻醉剂。氟烷对海藻酸盐诱导的谷氨酸释放的抑制作用不能通过增加海藻酸盐浓度来逆转,这表明氟烷不会在其受体上直接与海藻酸盐竞争。 [参考:41]

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