Bito H, Deisseroth K, Tsien R W
Department of Molecular and Cellular Physiology, Beckman Center for Molecular and Genetic Medicine, Stanford University School of Medicine, California 94305-5426, USA.
Cell. 1996 Dec 27;87(7):1203-14. doi: 10.1016/s0092-8674(00)81816-4.
While changes in gene expression are critical for many brain functions, including long-term memory, little is known about the cellular processes that mediate stimulus-transcription coupling at central synapses. In studying the signaling pathways by which synaptic inputs control the phosphorylation state of cyclic AMP-responsive element binding protein (CREB) and determine expression of CRE-regulated genes, we found two important Ca2+/calmodulin (CaM)-regulated mechanisms in hippocampal neurons: a CaM kinase cascade involving nuclear CaMKIV and a calcineurin-dependent regulation of nuclear protein phosphatase 1 activity. Prolongation of the synaptic input on the time scale of minutes, in part by an activity-induced inactivation of calcineurin, greatly extends the period over which phospho-CREB levels are elevated, thus affecting induction of downstream genes.
虽然基因表达的变化对包括长期记忆在内的许多脑功能至关重要,但对于在中枢突触中介导刺激-转录偶联的细胞过程却知之甚少。在研究突触输入控制环磷酸腺苷反应元件结合蛋白(CREB)磷酸化状态并决定CRE调节基因表达的信号通路时,我们在海马神经元中发现了两种重要的钙/钙调蛋白(CaM)调节机制:一种涉及核CaMKIV的CaM激酶级联反应,以及一种钙调神经磷酸酶依赖性的核蛋白磷酸酶1活性调节。在数分钟的时间尺度上延长突触输入,部分是通过钙调神经磷酸酶的活性诱导失活,极大地延长了磷酸化CREB水平升高的时间,从而影响下游基因的诱导。