Opioid Effects on 45Ca2+ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture
Opioid Effects on 45Ca2+ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture
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DOI：
10.1046/j.1471-4159.1997.68020517.x
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发表时间：
1997-02
影响因子：
4.7
通讯作者：
M. Vlaskovska;M. Schramm;I. Nylander;L. Kasakov;Z. You;M. Herrera-Marschitz;L. Terenius
中科院分区：
文献类型：
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作者：
M. Vlaskovska;M. Schramm;I. Nylander;L. Kasakov;Z. You;M. Herrera-Marschitz;L. Terenius
摘要：方便地从新生动物制备的大鼠皮质原代培养物被用于研究阿片类物质对⁴⁵Ca²⁺摄取和谷氨酸释放的影响。由谷氨酸或N - 甲基 - D - 天冬氨酸（NMDA）处理诱导的⁴⁵Ca²⁺摄取在很大程度上被NMDA拮抗剂MK - 801阻断。K⁺去极化诱导的⁴⁵Ca²⁺摄取也被MK - 801降低，这表明该作用是由谷氨酸释放介导的。直接分析证实谷氨酸和天冬氨酸确实被释放。强啡肽原系统的阿片肽也被释放，并且这些或其他肽具有功能活性，因为纳洛酮处理增加了谷氨酸释放以及去极化诱导的⁴⁵Ca²⁺摄取。对μ - 、κ - 和δ - 受体有选择性的阿片激动剂抑制了由K⁺去极化诱导的⁴⁵Ca²⁺摄取。低浓度的MK - 801和阿片激动剂的组合导致对K⁺诱导的⁴⁵Ca²⁺摄取的累加抑制。结果表明，该系统可用作体外中枢神经系统模型，用于研究在急性以及可能还有慢性阿片类药物治疗下阿片类物质对谷氨酸释放和Ca²⁺摄取的调节。
Abstract: Primary cultures of rat cortex, conveniently prepared from newborn animals, were used to study opioid effects on 45Ca2+ uptake and glutamate release. 45Ca2+ uptake, induced by treatment with glutamate or NMDA, was largely blocked by the NMDA antagonist MK‐801. K+ depolarization‐induced 45Ca2+ uptake was also reduced by MK‐801, indicating that the effect was mediated by glutamate release. Direct analysis verified that glutamate, and aspartate, were indeed released. Opioid peptides of the prodynorphin system were also released and these, or other peptides, were functionally active, because naloxone treatment increased glutamate release, as well as the 45Ca2+ uptake induced by depolarization. Opioid agonists, selective for μ‐, κ‐, and δ‐receptors, inhibited the 45Ca2+ uptake induced by K+ depolarization. The combination of low concentrations of MK‐801 and opioid agonists resulted in additive inhibition of K+‐ induced 45Ca2+ uptake. The results indicate that this system may be useful as an in vitro CNS model for studying modulation by opioids of glutamate release and Ca2+ uptake under acute, and perhaps also chronic, opiate treatment.