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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Chronic nicotine exposure selectively activates a carrier-mediated release of endogenous glutamate and aspartate from rat hippocampal synaptosomes
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Chronic nicotine exposure selectively activates a carrier-mediated release of endogenous glutamate and aspartate from rat hippocampal synaptosomes

机译：慢性尼古丁暴露选择性激活了载体介导的大鼠海马突触小体内源性谷氨酸和天冬氨酸的释放

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摘要

The effect of chronic nicotine treatment on the release of endogenous glutamate (GLU), aspartate (ASP) and GABA evoked in vitro by KCl, 4-aminopyridine (4AP) and nicotinic agonists in synaptosomes of rat hippocampus was investigated. Rats were chronically administered with nicotine bitartrate or saline vehicle each for 14 days using osmotic mini-pumps. Hippocampal synaptosomes were stimulated with KCl, 4AP, nicotine or with choline (Ch) and 5-iodo-A-85380 dihydrochloride (5IA85380). The GLU and ASP overflow evoked by Ch, nicotine, KCl and 4AP were increased in treated animals while the nicotine-evoked GABA overflow was reduced and that evoked by Ch, KCl and 4AP was unaffected. The 5IA85380-evoked overflow of the three aminoacids (AAs) was always reduced. The increase of ASP and GLU overflow evoked by KCl, 4AP or Ch was blocked by dl-threo-β-benzyloxyaspartic acid (dl-TBOA), a carrier transporter inhibitor, and by inhibitors of the Na +/Ca 2+ exchangers 2-[[4-[(4-nitrophenyl)methoxy]phenyl]methyl]-4-thiazolidinecarboxylic acid ethyl ester (SN-6) and 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea mesylate (KB-R7943). In conclusion long-term nicotine treatment may selectively increase GLU and ASP overflow elicited by KCl, 4AP and Ch through the activation of a carrier-mediated release mechanism and completely abolished the stimulatory effects of α4β2 nAChRs which modulate the release of all the three AA.
机译：研究了慢性尼古丁治疗对大鼠海马突触体中KCl，4-氨基吡啶（4AP）和烟碱激动剂体外诱发的内源性谷氨酸（GLU），天冬氨酸（ASP）和GABA释放的影响。使用渗透性微型泵对大鼠长期给予酒石酸尼古丁或生理盐水，持续14天。用KCl，4AP，烟碱或胆碱（Ch）和5-碘-A-85380二盐酸盐（5IA85380）刺激海马突触体。 Ch，尼古丁，KCl和4AP引起的GLU和ASP溢出在治疗的动物中增加，而尼古丁引起的GABA溢出减少，而Ch，KCl和4AP引起的GLU和ASP溢出不受影响。 5IA85380引起的三个氨基酸（AA）的溢出总是减少的。由KCl，4AP或Ch引起的ASP和GLU溢出的增加被载体转运蛋白抑制剂dl-苏-β-苄氧基天冬氨酸（dl-TBOA）以及Na + / Ca 2+交换子的抑制剂2阻止了2- [[4-[（4-硝基苯基甲氧基）苯基]甲基] -4-噻唑烷羧酸乙酯（SN-6）和2- [2- [4-（4-硝基苄氧基）苯基]乙基]异硫脲甲磺酸酯（KB -R7943）。总之，长期烟碱治疗可能通过激活载体介导的释放机制选择性地增加由KCl，4AP和Ch引起的GLU和ASP溢流，并完全消除了α4β2nAChRs刺激所有三种AA释放的刺激作用。

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