Evidence map›Paper›PMID 41417164›Full record

ArticleNeuroscience bulletin2026

GluA1 C80 Peptide Impairs Short-Term Spatial Memory in Mice by Interfering with the 4.1N Binding Site.

Yongfeng Li, Jinpeng Wang, Xiaoya Zhang, Junzhao Li, Kongjie Lu, Zhaodi Liu, Bizheng Wang, Xuewei Yang, Yong Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Yongfeng Li *Neuroscience 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.
Jinpeng Wang *Neuroscience 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.
Xiaoya ZhangNeuroscience 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.
Junzhao LiNeuroscience 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.
Kongjie LuNeuroscience 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.
Zhaodi LiuNeuroscience 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.
Bizheng WangNeuroscience 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.
Xuewei YangDepartment of Endocrinology, Peking University First Hospital, Beijing, 100034, China.
Yong ZhangNeuroscience 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. yongzhang@hsc.pku.edu.cn.ORCID http://orcid.org/0000-0001-8765-7037

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Memory, Short-TermPeptide FragmentsReceptors, AMPASpatial MemoryAnimalsBinding SitesCA1 Region, HippocampalLong-Term PotentiationMaleMiceMice, Inbred C57BLPeptide FragmentsReceptors, AMPAAMPARsGluA1 C80 peptideLearning and memoryLong-term potentiationSpatial memorySynaptic plasticity

Identifiers

PMID41417164
PMCPMC13221514

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.