ArticleNeuroscience bulletin2026
PTPRO Governs Synaptic Density, Long-Term Potentiation and Cognitive Function In Vivo.
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.
What it found
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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.
The trial behind it
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Authors and funding
15 authors.
Funding
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Abstract
Protein Tyrosine Phosphatase Receptor Type O (PTPRO) is a synaptic cell adhesion molecule that is essential for synapse formation in vitro; however, its in vivo role remains unclear. Using PTPRO-knockout mice, we found that PTPRO deletion reduced the number of synapses and impaired both excitatory and inhibitory synaptic transmission. PTPRO knockout also disrupted hippocampal long-term potentiation and caused learning and memory deficits in the water maze as well as in fear conditioning. Notably, overexpression of the N-terminal extracellular domain of PTPRO rescued the frequencies of miniature excitatory postsynaptic currents and inhibitory postsynaptic currents, indicating that this domain is required to regulate synapse number and transmission. Collectively, these data demonstrate that PTPRO is essential for maintaining synapse number, synaptic transmission, long-term potentiation, and learning and memory functions in vivo.
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Registered trials
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