N-甲基-D-天冬氨酸受体的基因缺失抑制了两种不同类型中枢神经元中的γ-氨基丁酸能突触传递。
Genetic deletion of NMDA receptors suppresses GABAergic synaptic transmission in two distinct types of central neurons.
作者信息
Gu Xinglong, Lu Wei
机构信息
Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.
Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.
出版信息
Neurosci Lett. 2018 Mar 6;668:147-153. doi: 10.1016/j.neulet.2018.01.024. Epub 2018 Feb 3.
Abstract
NMDA-type ionotropic glutamate receptors (NMDARs) play an important role in the regulation of synapse development and function in the brain. Recently we have shown that NMDARs are critical for GABAergic synapse development in developing hippocampal neurons. However, it remains unclear whether NMDARs are important for establishment of GABAergic synaptic transmission in other types of neurons in the brain. Here we report that in both cortical pyramidal neurons and midbrain dopamine neurons in ventral tegmental area (VTA), genetic deletion of the GluN1 subunit, which is required for assembly of functional NMDARs, leads to a strong reduction of GABAergic synaptic transmission. These data demonstrate that NMDARs play an important role in the development of GABAergic synaptic transmission in two types of neurons with distinct developmental origins, and suggest that NMDARs are commonly involved in development of GABAergic synaptic transmission in different types of neurons in the brain.
摘要
N-甲基-D-天冬氨酸（NMDA）型离子otropic谷氨酸受体（NMDARs）在大脑突触发育和功能的调节中起重要作用。最近我们发现，NMDARs对发育中的海马神经元的GABA能突触发育至关重要。然而，NMDARs对大脑中其他类型神经元的GABA能突触传递的建立是否重要仍不清楚。在这里我们报告，在皮层锥体神经元和腹侧被盖区（VTA）的中脑多巴胺神经元中，功能性NMDARs组装所必需的GluN1亚基的基因缺失导致GABA能突触传递的强烈减少。这些数据表明，NMDARs在具有不同发育起源的两种神经元的GABA能突触传递发育中起重要作用，并表明NMDARs通常参与大脑中不同类型神经元的GABA能突触传递发育。
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