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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Alterations of striatal neurotransmitter release in aquaporin-4 deficient mice: An in vivo microdialysis study.
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Alterations of striatal neurotransmitter release in aquaporin-4 deficient mice: An in vivo microdialysis study.

机译:Aquaporin-4缺陷型小鼠纹状体神经递质释放的变化:一项体内微透析研究。

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Our previous investigation has demonstrated that the lack of aquaporin-4 (AQP4) expressions in mice is paralleled by sex- and region-specific abnormalities in neurotransmission. In the present study, we examined the effect of AQP4 deficiency on release of neurotransmitters in mouse striatum using in vivo microdialysis after high K(+) stimulus. The results showed that neurotransmitter releases under the basal and K(+)-stimulated conditions in the striatum of wildtype mice were similar to AQP4 knockout mice, except for taurine, when measured at 24h after microdialysis surgery. However, the basal extracellular levels of dopamine and its metabolites were significantly increased in knockout mice, followed by reduced or no response to depolarizing stimuli when measured at 7 d after surgery. In addition, it was found that there were higher responses of amino acids to high K(+) stimulus in knockout mice. This experiment provides the in vivo evidence that AQP4 participates in the regulation of neurotransmitter release induced by depolarizing stimuli.
机译:我们以前的研究表明,小鼠中缺乏aquaporin-4(AQP4)的表达与神经传递中的性别和区域特异性异常平行。在本研究中,我们使用高K(+)刺激后体内微透析检查了AQP4缺乏对小鼠纹状体神经递质释放的影响。结果表明,在微透析手术后24小时测量时,野生型小鼠纹状体在基础和K(+)刺激的纹状体中神经递质的释放与AQP4敲除小鼠相似,但牛磺酸除外。然而,基因敲除小鼠的基础细胞外多巴胺水平及其代谢物显着增加,随后在术后7 d测量对去极化刺激的反应降低或没有反应。此外,发现在敲除小鼠中氨基酸对高K(+)刺激的反应更高。该实验提供了体内证据,表明AQP4参与了去极化刺激诱导的神经递质释放的调节。

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