激發(fā)性和抑制性突觸數(shù)量之間必須保持很好的平衡，神經(jīng)回路才能發(fā)揮功能,。人們對突觸,、尤其是抑制性突觸依賴于活性的形成中所涉及的細胞內(nèi)分子信號通道基本上不了解。
一項新的研究發(fā)現(xiàn),，轉(zhuǎn)錄因子Npas4在腦細胞中起一個“主開關(guān)”作用,，維持突觸激發(fā)和抑制之間的體內(nèi)平衡，該平衡被認為在如自閉癥,、癲癇癥和精神分裂癥等神經(jīng)疾病中受到破壞,。Npas4通過調(diào)控超過200個依賴于活性的基因的表達來發(fā)揮作用,，這些基因反過來又控制由GABA調(diào)控的突觸（它們形成激發(fā)性神經(jīng)元）的數(shù)量。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
