Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
Learn Mem. 2012 Aug 16;19(9):391-400. doi: 10.1101/lm.025304.111.
The search for molecules that restrict synaptic plasticity in the brain has focused primarily on sensory systems during early postnatal development, as critical periods for inducing plasticity in sensory regions are easily defined. The recent discovery that Schaffer collateral inputs to hippocampal area CA2 do not readily support canonical activity-dependent long-term potentiation (LTP) serves as a reminder that the capacity for synaptic modification is also regulated anatomically across different brain regions. Hippocampal CA2 shares features with other similarly "LTP-resistant" brain areas in that many of the genes linked to synaptic function and the associated proteins known to restrict synaptic plasticity are expressed there. Add to this a rich complement of receptors and signaling molecules permissive for induction of atypical forms of synaptic potentiation, and area CA2 becomes an ideal model system for studying specific modulators of brain plasticity. Additionally, recent evidence suggests that hippocampal CA2 is instrumental for certain forms of learning, memory, and social behavior, but the links between CA2-enriched molecules and putative CA2-dependent behaviors are only just beginning to be made. In this review, we offer a detailed look at what is currently known about the synaptic plasticity in this important, yet largely overlooked component of the hippocampus and consider how the study of CA2 may provide clues to understanding the molecular signals critical to the modulation of synaptic function in different brain regions and across different stages of development.
大脑中限制突触可塑性的分子的研究主要集中在出生后早期的感觉系统上，因为在感觉区域诱导可塑性的关键时期很容易定义。最近的发现表明，海马区 CA2 的 Schaffer 侧枝输入不容易支持经典的活性依赖性长时程增强（LTP），这提醒人们，不同脑区的突触修饰能力也受到解剖结构的调节。海马 CA2 与其他类似的“LTP 抵抗”脑区具有共同特征，许多与突触功能相关的基因以及已知限制突触可塑性的相关蛋白都在那里表达。此外，丰富的受体和信号分子补充了诱导非典型形式的突触增强的可能性，使得 CA2 区域成为研究大脑可塑性特定调节剂的理想模型系统。此外，最近的证据表明，海马 CA2 对某些形式的学习、记忆和社会行为至关重要，但 CA2 丰富的分子和假定的 CA2 依赖性行为之间的联系才刚刚开始建立。在这篇综述中，我们详细介绍了目前已知的海马体这一重要但在很大程度上被忽视的组成部分中的突触可塑性，并探讨了 CA2 的研究如何为理解对不同脑区和不同发育阶段的突触功能调节至关重要的分子信号提供线索。
