Data from: Impaired spatial memory codes in a mouse model of Rett syndrome

The Mecp2+/-mouse model recapitulates many phenotypes of patients with Rett syndrome (RTT), including learning and memory deficits. It is unknown, however, how the disease state alters memory circuit functions in vivoin RTT mice. Here we recorded from hippocampal place cells, which are thought to encode spatial memories, in freely moving RTT mice and littermate controls. We found that place cells in RTT mice are impaired in their experience-dependent increase of spatial information. This impairment is accompanied by an enhanced baseline firing synchrony of place cells within ripple oscillations during rest, which consequently occludes the increase in synchrony after a novel experience. Behaviorally, contextual memory is normal at short but not long time scale in RTT mice. Our results suggest that hypersynchrony interferes with memory consolidation and leads to impaired spatial memory codes in RTT mice, providing a possible circuit mechanism for memory deficits in Rett Syndrome.Mecp2杂合子小鼠模型（Mecp2+/- mouse model）可复现瑞特综合征（Rett syndrome, RTT）患者的多种表型，包括学习与记忆缺陷。然而目前尚不清楚，瑞特综合征小鼠体内的疾病状态如何改变记忆环路的在体功能。本研究对自由活动的瑞特综合征小鼠及同窝对照小鼠的海马位置细胞（place cells）进行了记录，这类细胞被认为参与编码空间记忆。研究发现，瑞特综合征小鼠的位置细胞在依赖经验的空间信息增益方面存在功能损伤。该功能损伤伴随静息状态下涟漪振荡（ripple oscillations）期间位置细胞的基础放电同步性增强，进而阻碍了新经验诱导下的同步性提升。行为学层面，瑞特综合征小鼠的情境记忆在短时程下表现正常，但长时程则出现异常。本研究结果表明，神经元过度同步化会干扰记忆巩固过程，并导致瑞特综合征小鼠的空间记忆编码受损，为瑞特综合征患者的记忆缺陷提供了一种潜在的环路机制。