激发性和抑制性突触数量之间必须保持很好的平衡，神经回路才能发挥功能。人们对突触、尤其是抑制性突触依赖于活性的形成中所涉及的细胞内分子信号通道基本上不了解。
一项新的研究发现，转录因子Npas4在脑细胞中起一个“主开关”作用，维持突触激发和抑制之间的体内平衡，该平衡被认为在如自闭症、癫痫症和精神分裂症等神经疾病中受到破坏。Npas4通过调控超过200个依赖于活性的基因的表达来发挥作用，这些基因反过来又控制由GABA调控的突触（它们形成激发性神经元）的数量。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 455, 1198-1204 (30 October 2008) | doi:10.1038/nature07319
Activity-dependent regulation of inhibitory synapse development by Npas4
Yingxi Lin1, Brenda L. Bloodgood1, Jessica L. Hauser1,4, Ariya D. Lapan2, Alex C. Koon1,4, Tae-Kyung Kim1, Linda S. Hu1, Athar N. Malik1,3 & Michael E. Greenberg1
1 F. M. Kirby Neurobiology Center, Children's Hospital and Departments of Neurology and Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
2 Program in Biological and Biomedical Sciences, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
3 Program in Neuroscience, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
4 Present addresses: Baylor College of Medicine, Medical Scientist Training Program, One Baylor Plaza Suite N201, MS:BCM215, Houston, Texas 77030-7498, USA (J.L.H.); University of Massachusetts Medical School, Lazare Medical Research Building, Room 760C, 364 Plantation Street, Worcester, Massachusetts 06105, USA (A.C.K.).
Neuronal activity regulates the development and maturation of excitatory and inhibitory synapses in the mammalian brain. Several recent studies have identified signalling networks within neurons that control excitatory synapse development. However, less is known about the molecular mechanisms that regulate the activity-dependent development of GABA (-aminobutyric acid)-releasing inhibitory synapses. Here we report the identification of a transcription factor, Npas4, that plays a role in the development of inhibitory synapses by regulating the expression of activity-dependent genes, which in turn control the number of GABA-releasing synapses that form on excitatory neurons. These findings demonstrate that the activity-dependent gene program regulates inhibitory synapse development, and suggest a new role for this program in controlling the homeostatic balance between synaptic excitation and inhibition.
