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Péptido GluA1 C80 altera la memoria espacial a corto plazo en ratones al interferir con el sitio de unión 4.1N
Yongfeng Li1,2, Jinpeng Wang1,2, Xiaoya Zhang1,2
1Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of China, Beijing, 100083, China.
Abstract:
AMPA receptors mediate the majority of excitatory synaptic transmission in the central nervous system, and are essential for LTP/LTD through insertion into/removal from postsynaptic density. Experimental manipulation (pharmacological, genetic) of AMPA receptors affects synaptic plasticity and has important implications for learning and memory and neurological diseases. We found that bilateral expression of the GluA1 C80 peptide in the dorsal hippocampus CA1 region acutely blocked endogenous GluA1 function, significantly affected the synaptic plasticity, which led to impairments in short-term spatial memory but not long-term spatial memory in mice. Mechanistically, our results revealed that the GluA1 C80 peptide might impair LTP and short-term spatial memory through interference of the binding between GluA1 to 4.1N. Our study suggests that the GluA1 C80 peptide could serve as a useful tool for acute manipulation of endogenous AMPA receptors in a brain region-specific manner in vivo.
