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首页> 外文期刊>Addiction biology >Lesions of nucleus accumbens affect morphine-induced release of ascorbic acid and GABA but not of glutamate in rats.
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Lesions of nucleus accumbens affect morphine-induced release of ascorbic acid and GABA but not of glutamate in rats.

机译：伏伏核损伤影响吗啡诱导的大鼠抗坏血酸和GABA的释放，但不影响谷氨酸的释放。

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Our previous studies have shown that local perfusion of morphine causes an increase of extracellular ascorbic acid (AA) levels in nucleus accumbens (NAc) of freely moving rats. Lines of evidence showed that glutamatergic and GABAergic were associated with morphine-induced effects on the neurotransmission of the brain, especially on the release of AA. In the present study, the effects of morphine on the release of extracellular AA, gamma-aminobutyric acid (GABA) and glutamate (Glu) in the NAc following bilateral NAc lesions induced by kainic acid (KA) were studied by using the microdialysis technique, coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD) and fluorescent detection (HPLC-FD). The results showed that local perfusion of morphine (100 microM, 1 mM) in NAc dose-dependently increased AA and GABA release, while attenuated Glu release in the NAc. Naloxone (0.4 mM) pretreated by local perfusion to the NAc, significantly blocked the effects of morphine. After NAc lesion by KA (1 microg), morphine-induced increase in AA and GABA were markedly eliminated, while decrease in Glu was not affected. The loss effect of morphine on AA and GABA release after KA lesion could be recovered by GABA agonist, musimol. These results indicate that morphine-induced AA release may be mediated at least by micro-opioid receptor. Moreover, this effect of morphine possibly depend less on the glutamatergic afferents, but more on the GABAergic circuits within this nucleus. Finally, AA release induced by local perfusion of morphine may be GABA-receptor mediated and synaptically localized in the NAc.
机译：我们以前的研究表明，吗啡的局部灌注会导致自由运动大鼠伏伏核（NAc）的细胞外抗坏血酸（AA）水平升高。证据表明，谷氨酸能和GABA能与吗啡诱导的对大脑神经传递的影响有关，特别是与AA的释放有关。在本研究中，通过微透析技术研究了吗啡对海藻酸（KA）引起的双侧NAc损伤后NAc中胞外AA，γ-氨基丁酸（GABA）和谷氨酸（Glu）释放的影响，结合了具有电化学检测（HPLC-ECD）和荧光检测（HPLC-FD）的高效液相色谱。结果表明，在NAc中局部灌注吗啡（100 microM，1 mM）剂量依赖性地增加了AA和GABA的释放，而减弱了NAc中的Glu释放。通过局部灌注NAc预处理的纳洛酮（0.4 mM）显着阻断了吗啡的作用。 KA（1微克）的NAc损伤后，吗啡引起的AA和GABA的增加被明显消除，而Glu的减少不受影响。 GABA激动剂musimol可恢复吗啡对KA损伤后AA和GABA释放的损失作用。这些结果表明吗啡诱导的AA释放至少可以由微阿片受体介导。此外，吗啡的这种作用可能较少地依赖于谷氨酸能的传入，但是更多地依赖于该核内的GABA能回路。最后，由吗啡的局部灌注诱导的AA释放可能是GABA-受体介导的并且突触地位于NAc中。

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