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Enhancing GluN2A-type NMDA receptors impairs long-term synaptic plasticity and learning and memory - PubMed
Source: pubmed.ncbi.nlm.nih.gov
Article summary:
1. A rare variant in the NMDAR subunit GluN2A (K879R) was identified in a patient with intellectual disability.
2. Expression of GluN2A_K879R in mouse hippocampal CA1 neurons enhanced the excitatory postsynaptic currents mediated by GluN2A-NMDAR but suppressed those mediated by GluN2B-NMDAR and the AMPA receptor.
3. GluN2A_K879R knock-in mice showed impaired learning and memory, as well as severely impaired long-term synaptic plasticity.
Article analysis:
The article is generally reliable and trustworthy, as it is based on research conducted by a team of experts from multiple institutions, including universities and hospitals. The authors have provided evidence to support their claims, such as data from experiments conducted on mice, which adds credibility to their findings. Furthermore, the authors have provided references to other relevant studies that support their conclusions.
However, there are some potential biases that should be noted. For example, the study only focused on one particular mutation in the NMDAR subunit GluN2A (K879R), so it may not be applicable to other mutations or variants of this gene. Additionally, since the study was conducted using animal models, its results may not be directly applicable to humans. Finally, while the authors have provided references to other relevant studies that support their conclusions, they do not explore any counterarguments or alternative explanations for their findings.