Guo Rui, Ge Rongjing, Zhao Shidi, Liu Yulong, Zhao Xin, Huang Li, Guan Sodong, Lu Wei, Cui Shan, Wang Shirlene, Wang Jin-Hui
Department of Pathophysiology, Bengbu Medical CollegeAnhui, China.
School of Pharmacy, Qingdao UniversityQingdao, China.
Front Cell Neurosci. 2017 Jun 14;11:168. doi: 10.3389/fncel.2017.00168. eCollection 2017.
Associative memory is essential for cognition, in which associative memory cells and their plasticity presumably play important roles. The mechanism underlying associative memory extinction vs. maintenance remains unclear, which we have studied in a mouse model of cross-modal associative learning. Paired whisker and olfaction stimulations lead to a full establishment of odorant-induced whisker motion in training day 10, which almost disappears if paired stimulations are not given in a week, and then recovers after paired stimulation for an additional day. In mice that show associative memory, extinction and recovery, we have analyzed the dynamical plasticity of glutamatergic neurons in layers II-III of the barrel cortex and layers IV-V of the motor cortex. Compared with control mice, the rate of evoked spikes as well as the amplitude and frequency of excitatory postsynaptic currents increase, whereas the amplitude and frequency of inhibitory postsynaptic currents (IPSC) decrease at training day 10 in associative memory mice. Without paired training for a week, these plastic changes are persistent in the barrel cortex and decayed in the motor cortex. If paired training is given for an additional day to revoke associative memory, neuronal plasticity recovers in the motor cortex. Our study indicates persistent neuronal plasticity in the barrel cortex for cross-modal memory maintenance as well as the dynamical change of neuronal plasticity in the motor cortex for memory retrieval and extinction. In other words, the sensory cortices are essential for long-term memory while the behavior-related cortices with the inability of memory retrieval are correlated to memory extinction.
联合记忆对认知至关重要，其中联合记忆细胞及其可塑性可能起着重要作用。联合记忆消退与维持的潜在机制仍不清楚，我们在跨模态联合学习的小鼠模型中对此进行了研究。在训练第10天，配对的胡须和嗅觉刺激会导致气味诱导的胡须运动完全建立，如果一周内不给予配对刺激，这种运动几乎消失，然后在额外一天的配对刺激后恢复。在表现出联合记忆、消退和恢复的小鼠中，我们分析了桶状皮层II-III层和运动皮层IV-V层谷氨酸能神经元的动态可塑性。与对照小鼠相比，在联合记忆小鼠的训练第10天，诱发尖峰的速率以及兴奋性突触后电流的幅度和频率增加，而抑制性突触后电流（IPSC）的幅度和频率降低。在没有配对训练一周的情况下，这些可塑性变化在桶状皮层中持续存在，而在运动皮层中衰减。如果给予额外一天的配对训练以消除联合记忆，运动皮层中的神经元可塑性会恢复。我们的研究表明，桶状皮层中存在持续的神经元可塑性以维持跨模态记忆，而运动皮层中神经元可塑性的动态变化与记忆检索和消退相关。换句话说，感觉皮层对长期记忆至关重要，而与行为相关但无法进行记忆检索的皮层与记忆消退相关。
