Effects of inhalation anesthetics of Kainate-induced glutamate release from cerebellar granule cells.
Effects of inhalation anesthetics of Kainate-induced glutamate release from cerebellar granule cells.
复制标题
吸入麻醉剂对红藻氨酸诱导的小脑颗粒细胞谷氨酸释放的影响。
DOI:
10.1016/0024-3205(96)00102-6
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发表时间:
1996
期刊:
影响因子:
6.1
通讯作者:
Baker,RC
中科院分区:
文献类型:
--
作者:
Zhu,S;Baker,RC
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.