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首页> 外文期刊>Addiction biology >Genetic differences in the modulation of accumbal glutamate and γ-amino butyric acid levels after cocaine-induced reinstatement
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Genetic differences in the modulation of accumbal glutamate and γ-amino butyric acid levels after cocaine-induced reinstatement

机译：可卡因恢复后的谷氨酸和γ-氨基丁酸水平调节的遗传差异

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摘要

The Lewis (LEW) and Fischer 344 (F344) inbred rat strains are frequently used to study the role of genetic factors in vulnerability to drug addiction and relapse. Glutamate and γ-amino butyric acid (GABA) transmission are significantly altered after cocaine-induced reinstatement, although whether LEW and F344 rats differ in their accumbal glutamate and GABA responsiveness to cocaine-induced reinstatement remains unknown. To investigate this, we measured by in vivo microdialysis extracellular glutamate and GABA levels in the core division of the nucleus accumbens after extinction of cocaine self-administration and during cocaine-induced reinstatement (7.5 mg/kg, i.p.) in these two strains of rats. No strain differences were evident in cocaine self-administration or extinction behavior, although cocaine priming did induce a higher rate of lever pressing in LEW compared with F344 rats. After extinction, F344 rats that self-administered cocaine had less GABA than the saline controls, while the glutamate levels remained constant in both strains. There was more accumbal glutamate after cocaine priming in LEW rats that self-administered cocaine, while GABA levels were unaffected. By contrast, GABA increased transiently in F344 rats that self-administered cocaine, while glutamate levels were unaltered. In F344 saline controls, cocaine priming provoked contrasting effects in glutamate and GABA levels, inducing a delayed increase in glutamate and a delayed decrease in GABA levels. These amino acids were unaffected by cocaine priming in LEW saline rats. Together, these results suggest that genetic differences in cocaine-induced reinstatement reflect different responses of the accumbal GABA and glutamate systems to cocaine priming.
机译：Lewis（LEW）和Fischer 344（F344）自交系大鼠品系经常用于研究遗传因素在药物成瘾和复发易感性中的作用。尽管可卡因引起的恢复后谷氨酸和γ-氨基丁酸（GABA）的传递发生了显着改变，但尚不清楚LEW和F344大鼠的累积谷氨酸和GABA对可卡因引起的恢复的反应性是否仍然未知。为了对此进行研究，我们通过体内微透析在这两种大鼠的可卡因自我给药灭绝后和可卡因诱导的恢复剂量（7.5 mg / kg，腹膜内）中通过伏安核伏核核心区的细胞外谷氨酸和GABA水平进行了测量。 。尽管可卡因引发与F344大鼠相比确实在LEW中引起较高的杠杆按压率，但在可卡因自我给药或绝灭行为中没有明显的菌株差异。灭绝后，自我施用可卡因的F344大鼠的GABA含量低于生理盐水对照组，而两种菌株的谷氨酸水平保持恒定。在LEW大鼠中，可卡因引发后的累积谷氨酸盐含量高于可卡因，而GABA水平未受影响。相比之下，在自行服用可卡因的F344大鼠中，GABA瞬时升高，而谷氨酸水平未改变。在F344盐溶液对照中，可卡因引发引发了谷氨酸和GABA水平的反作用，导致谷氨酸水平的延迟增加和GABA水平的延迟下降。这些氨基酸不受LEW盐水大鼠中可卡因引发的影响。总之，这些结果表明，可卡因诱导的恢复的遗传差异反映了累积性GABA和谷氨酸系统对可卡因引发的不同反应。

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