Marie Hélène, Morishita Wade, Yu Xiang, Calakos Nicole, Malenka Robert C
Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Neuron. 2005 Mar 3;45(5):741-52. doi: 10.1016/j.neuron.2005.01.039.
The transcription factor CREB is critical for several forms of experience-dependent plasticity in a range of species and is commonly activated in neurons by calcium/calmodulin-dependent protein kinase IV (CaMKIV). Surprisingly, little is known about the neural circuit adaptations caused by activation of CaMKIV and CREB. Here, we use viral-mediated gene transfer in vivo to examine the consequences of acute expression of constitutively active forms of CaMKIV and CREB on synaptic function in the rodent hippocampus. Acute expression of active CaMKIV or CREB caused an enhancement of both NMDA receptor-mediated synaptic responses and long-term potentiation (LTP). This was accompanied by electrophysiological and morphological changes consistent with the generation of "silent synapses," which provide an ideal substrate for further experience-dependent modifications of neural circuitry and which may also be important for the consolidation of long-term synaptic plasticity and memories.
转录因子CREB对于一系列物种中几种形式的经验依赖性可塑性至关重要，并且通常在神经元中由钙/钙调蛋白依赖性蛋白激酶IV（CaMKIV）激活。令人惊讶的是，对于由CaMKIV和CREB激活引起的神经回路适应性知之甚少。在这里，我们在体内使用病毒介导的基因转移来检查组成型活性形式的CaMKIV和CREB的急性表达对啮齿动物海马体突触功能的影响。活性CaMKIV或CREB的急性表达导致NMDA受体介导的突触反应和长时程增强（LTP）增强。这伴随着与“沉默突触”产生一致的电生理和形态学变化，“沉默突触”为神经回路的进一步经验依赖性修饰提供了理想的底物，并且对于长期突触可塑性和记忆的巩固也可能很重要。
