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Extensive studies have investigated the roles of tyrosine kinases in memory formation. However, there were few studies on PTPs. To date, learning has been shown to be defective only for mouse knock-outs of PTP\u03b1, leukocyte common antigen-related, or PTP\u03b4. A major limitation of these studies arises from their inability to distinguish an acute (biochemical) impairment of memory formation from a more chronic abnormality in neurodevelopment. From a behavioral screen for defective long-term memory, we found<jats:italic>chi<\/jats:italic>mutants to disrupt expression of the PTP10D protein tyrosine phosphatase gene. We show that<jats:italic>chi<\/jats:italic>mutants are normal for learning, early memory, and anesthesia-resistant memory, whereas long-term memory specifically is abolished. Significantly, induction of a heat shock-PTP10D<jats:sup>+<\/jats:sup>transgene before training fully rescues the memory defect of<jats:italic>chi<\/jats:italic>mutants, thereby demonstrating an acute role for PTP10D in behavioral plasticity. We show that PTP10D is widely expressed in the embryonic CNS and in the adult brain. Transgenic expression of upstream activating sequence-PTP10D<jats:sup>+<\/jats:sup>in mushroom bodies is sufficient to rescue the memory defect of<jats:italic>chi<\/jats:italic>mutants. Our data clearly demonstrate that signaling through PTP10D in mushroom bodies is critical for the formation of long-term memory.<\/jats:p>","DOI":"10.1523\/jneurosci.4054-06.2007","type":"journal-article","created":{"date-parts":[[2007,4,18]],"date-time":"2007-04-18T16:48:03Z","timestamp":1176914883000},"page":"4396-4402","source":"Crossref","is-referenced-by-count":17,"title":["Receptor-Like Tyrosine Phosphatase PTP10D Is Required for Long-Term Memory 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