About 5~12% of school-aged children suffer from the Attention-Deficit/Hyperactivity Disorder (ADHD). However, the core mechanism of ADHD remains unclear. G protein-coupled receptor kinase-interacting protein-1 (GIT1) has recently been reported to be associated with ADHD in human and the genetic deletion of GIT1 result in ADHD-like behaviors in mice. Mice lacking GIT1 shows a shift in neuronal excitation/inhibition (E/I) balance. However, the pricise mechanism for E/I imbalance and the role of neuron-glia interaction in GIT1 knockout (KO) mice have not been studied. Especially, a possible contribution of glial GABA and tonic inhibition mediated by astrocytic GABA release in the mouse model for ADHD remains unexplored. Therefore, we investigated the changes in the amount of GABA and degree of tonic inhibition in GIT1 KO mice. We observed a decreased glial GABA intensity in GIT1 KO mice compared to wild type (WT) mice and an attenuation of tonic current from cerebellar granule cells in GIT1 KO mice. Our study identifies the previously unknown mechanism of reduced astrocytic GABA and tonic inhibition in GIT1 lacking mice as a potential cause of hyperactivity disorder.

中文翻译：

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注意力缺陷/多动障碍（ADHD）小鼠模型小脑中胶质GABA的减少和强直抑制作用。

约5〜12％的学龄儿童患有注意力缺乏/多动症（ADHD）。然而，多动症的核心机制仍不清楚。最近有报道称，G蛋白偶联受体激酶相互作用蛋白1（GIT1）与人的ADHD相关，而GIT1的基因缺失导致小鼠出现ADHD样的行为。缺少GIT1的小鼠显示神经元兴奋/抑制（E / I）平衡发生变化。但是，尚未研究E / I失衡的确切机制以及GIT1基因敲除（KO）小鼠中神经元-神经胶质相互作用的作用。特别是，ADHD小鼠模型中神经胶质GABA和由星形胶质GABA释放介导的强直抑制的可能贡献尚待研究。因此，我们调查了GIT1 KO小鼠中GABA的量和滋补抑制程度的变化。我们观察到，与野生型（WT）小鼠相比，GIT1 KO小鼠的神经胶质GABA强度降低，而GIT1 KO小鼠的小脑颗粒细胞的强直电流减弱。我们的研究确定了缺乏GIT1的小鼠中减少星形细胞GABA和强直抑制的先前未知的机制，这是过度活跃症的潜在原因。