首页> 外文期刊>European Journal of Pharmacology: An International Journal >Different strains of rats show different sensitivity to block of long-term potentiation by nitric oxide synthase inhibitors.
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Different strains of rats show different sensitivity to block of long-term potentiation by nitric oxide synthase inhibitors.

机译:不同品系的大鼠对一氧化氮合酶抑制剂阻断长期增强的敏感性不同。

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摘要

Nitric oxide is presumed to play important roles in the induction of synaptic plasticity and learning. Previous publications, however, reported contradictory results. Block of nitric oxide synthase (NOS) has been shown to impair the induction of long-term potentiation of synaptic transmission in some studies. Other studies observed a partial block of long-term potentiation depending on experimental conditions, while yet other studies did not find an effect of NOS inhibitors under any conditions tested. Some reasons for these differences had been identified, e.g. the temperature of the slice buffer, the age of the animals, and the specific stimulation protocols used. Still, even when taking these parameters into account, not all results can be explained. The present study compares three strains of rats and observes large differences in sensitivity to nitric oxide synthase (NOS) blockers on the induction of long-term potentiation. While Wistar rats showed an almost complete block of long-term potentiation when using the NOS inhibitors 7-nitro-indazole (30 mg/kg ip) or 1-(2-trifluoromethylphenyl) imidazole (TRIM; 150 nmol/5 microl icv), 117+/-5 S.E.M. of % of baseline slope values of excitatory postsynaptic potentials. Sprague-Dawley and Long-Evans rats showed no or only weak effects of drugs on the induction of long-term potentiation (166+/-17 S.E.M. of % of baseline slopes in Sprague-Dawley rats, 173+/-24 S.E.M. of % of baseline values in Long-Evans rats). The results could explain at least some of the discrepancies of the efficacy of NOS inhibitors on synaptic plasticity that is found in the literature. Such large strain differences suggest that results from studies that use laboratory rats could have strain-dependent components and should be generalised cautiously.
机译:一氧化氮被认为在诱导突触可塑性和学习中起重要作用。但是,以前的出版物报道了矛盾的结果。一氧化氮合酶(NOS)的阻滞在某些研究中已显示出削弱突触传递长期增强的诱导作用。其他研究根据实验条件观察到部分长期增强作用,而其他研究未发现在任何测试条件下NOS抑制剂的作用。已经确定了造成这些差异的一些原因,例如切片缓冲液的温度,动物的年龄以及使用的特定刺激方案。尽管如此,即使考虑这些参数,也无法解释所有结果。本研究比较了三种大鼠,观察到对一氧化氮合酶(NOS)阻滞剂的敏感性在长期增强诱导上的巨大差异。当使用NOS抑制剂7-硝基-吲唑(30 mg / kg ip)或1-(2-三氟甲基苯基)咪唑(TRIM; 150 nmol / 5 microl icv)时,Wistar大鼠显示出几乎完全的长期增强阻断作用, 117 +/- 5扫描电镜兴奋性突触后电位的基线斜率值的百分比。 Sprague-Dawley和Long-Evans大鼠对长期增强的诱导没有或仅有微弱的作用(Sprague-Dawley大鼠基线斜率的166 +/- 17 SEM,%173 +/- 24 SEM Long-Evans大鼠的基线值)。该结果至少可以解释文献中发现的NOS抑制剂对突触可塑性的功效的某些差异。如此大的应变差异表明,使用实验室大鼠的研究结果可能具有应变依赖性成分,应谨慎推广。

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