{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:18:39Z","timestamp":1784557119578,"version":"3.55.0"},"reference-count":71,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:p>The double postnatal stress model (brief maternal separation plus sham injection daily applied from birth to weaning) induces metabolic alterations similar to type 2 diabetes in young-adult male mice. We verify whether 1) the stress also induces brain metabolic\u2013functional alterations connected to diabetes and 2) different alterations are modulated selectively by two stress-damaged endogenous systems (opioid- and\/or ACTH\u2013corticosteroid-linked). Here, diabetes-like metabolic plus neurophysiologic\u2013neurometabolic parameters are studied in adult mice following postnatal stress and drug treatment. Surprisingly, together with \u2018classic\u2019 diabetes-like alterations, the stress model induces in young-adult mice significantly enhanced brain neurometabolic\u2013neurophysiologic performances, consisting of decreased latency to flash-visual evoked potentials (\u2212\u223c8%); increased level (+\u223c40%) and reduced latency (\u2212\u223c30%) of NAD(P)H autofluorescence postsynaptic signals following electric stimuli; enhanced passive avoidance learning (+\u223c135% latency); and enhanced brain-derived neurotrophic factor level (+\u223c70%). Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTH\u2013corticosterone system hyper-functioning. Our stress model induces diabetes-like metabolic alterations coupled to enhanced brain neurometabolic\u2013neurophysiologic performances. Taken all together, these findings are compatible with an \u2018enduring acute-stress\u2019 reaction, which puts mice in favorable survival situations vs controls. However, prolonged hormonal\u2013metabolic imbalances are expected to also produce diabetes-like complications at later ages in stressed mice.<\/jats:p>","DOI":"10.1530\/joe-12-0369","type":"journal-article","created":{"date-parts":[[2012,10,9]],"date-time":"2012-10-09T22:39:08Z","timestamp":1349822348000},"page":"413-424","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":6,"title":["Enhanced brain performance in mice following postnatal stress"],"prefix":"10.1530","volume":"215","author":[{"given":"Alberto","family":"Loizzo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Santi 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