{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T02:18:41Z","timestamp":1779416321048,"version":"3.53.1"},"reference-count":42,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Oxytocin (OXT), a neuropeptide produced in the paraventricular nucleus (PVN) of the hypothalamus, regulates social behaviour, stress responses, and memory. Our previous studies demonstrated that intracerebroventricular administration of OXT ameliorates amyloid\u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2013induced cognitive deficits and that selective activation of PVN OXT neurons enhances memory performance. These findings suggest that endogenous OXT secretion is essential for normal memory processing and that its impairment may lead to cognitive dysfunction. To test this hypothesis, we generated oxytocin neuron\u2010specific conditional knockout (cKO) mice for the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010dependent activator protein for secretion 2 (CAPS2) by crossing\n                    <jats:italic>Caps2<\/jats:italic>\n                    \u2010floxed mice with oxytocin\u2010iCre mice. In these mice, OXT exocytosis was selectively impaired in OXT neurons. Behavioural analyses revealed that\n                    <jats:italic>Caps2<\/jats:italic>\n                    cKO mice exhibited deficits in long\u2010term memory in the novel object recognition test (NORT) and passive avoidance tests, whereas short\u2010term spatial memory assessed by the Y\u2010maze test remained unaffected. Electrophysiological recordings further showed that hippocampal long\u2010term potentiation was markedly attenuated in\n                    <jats:italic>Caps2<\/jats:italic>\n                    cKO mice. Consistently, phosphorylated ERK levels in the ventral hippocampus were significantly reduced following the NORT. These findings demonstrate that CAPS2\u2010dependent OXT release is critical for long\u2010term memory formation and hippocampal synaptic plasticity. Our results provide new insight into the physiological role of endogenous OXT signalling in cognitive function and suggest its potential relevance to the pathogenesis of memory disorders such as Alzheimer's disease.\n                  <\/jats:p>","DOI":"10.1111\/ejn.70530","type":"journal-article","created":{"date-parts":[[2026,5,9]],"date-time":"2026-05-09T01:39:22Z","timestamp":1778290762000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Oxytocin Neuron\u2010Specific CAPS2 Deficiency in Mice Impairs Hippocampal Plasticity and Long\u2010Term Memory Through Reduced ERK Phosphorylation in the Ventral hippocampus"],"prefix":"10.1111","volume":"63","author":[{"given":"Wakana","family":"Nagano","sequence":"first","affiliation":[{"name":"Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences Tokyo University of Science  Tokyo 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