Hyperactivity in mice lacking one allele of the glutamic acid decarboxylase 67 gene.
Hyperactivity in mice lacking one allele of the glutamic acid decarboxylase 67 gene.
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DOI：
10.1007/s12402-018-0254-0
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发表时间：
2018-12
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影响因子：
--
通讯作者：
Smith KM
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作者：
Smith KM
GABA 能中间神经元丢失、成熟延迟或谷氨酸能与 GABA 能信号传导失衡与多种神经精神疾病有关，包括抽动秽语综合征和注意力缺陷/多动障碍 (ADHD)。在精神分裂症中，已观察到小清蛋白 (PV)、生长抑素 (Sst) 和谷氨酸脱羧酶 (GAD) RNA 的减少，这似乎表明 PV 和 Sst 神经元成熟失败。在多动症（ADHD）合并症较高的抽动秽语综合征中，在受影响患者的基底神经节中观察到表达小清蛋白的神经元数量减少。此外，编码 GAD67 蛋白的 GAD1 基因的多态性与 ADHD 相关。我们检查了具有破坏的 Gad67 等位基因的小鼠（Gad67 GFP 敲入小鼠 (Gad67-GFP+/-)）是否表现出异常的运动行为或在高架十字迷宫中改变的焦虑行为。我们发现与对照同窝小鼠相比，Gad67-GFP+/- 小鼠表现出轻度过度活跃。
GABAergic interneuron loss, maturational delay, or imbalance of glutamatergic to GABAergic signaling has been implicated in several neuropsychiatric disorders including Tourette syndrome and attention-deficit/hyperactivity disorder (ADHD). In schizophrenia, decreases in Parvalbumin (PV), Somatostatin (Sst), and Glutamic Acid Decarboxylase (GAD) RNA have been observed and seem to indicate a failure in maturation in PV and Sst neurons. In Tourette syndrome, which has a high level of comorbid ADHD, reduced numbers of parvalbumin expressing neurons have been observed in the basal ganglia of affected patients. In addition, polymorphisms in the GAD1 gene that codes for GAD67 protein have been associated with ADHD. We have examined whether mice with a disrupted Gad67 allele, the Gad67 GFP knock-in mice (Gad67-GFP+/−), display abnormal locomotor behavior, or altered anxiety behavior on the elevated plus maze. We found that Gad67-GFP+/− mice displayed a mild hyperactivity compared to control littermates.