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https://www.selleckchem.com/products/c75.html Interestingly, only female ECMS mice at adulthood maintained juvenile-like OD plasticity as well as high NR2B expressions. Artificial increase in estradiol level in ECMS males via estradiol supplementary diminished this sex difference. Lastly, OD plasticity was abolished in adult ECMS females either performed with the bilateral ovariectomy in prepuberty, or directly infused with NR2B antagonist Ro 25-6981 into the visual cortex. Overall, our study demonstrates that early adverse experiences have a lasting effect on visual development of mice in a sex-dependent manner, which is mediated by the estradiol-NR2B pathway.The role of stress in the etiology of depression has been largely reported. In this line, exogenous glucocorticoids are employed to mimic the influence of stress on the development of depression. The N/OFQ-NOP receptor system has been implicated in the modulation of stress and emotional behaviors. In fact, the blockade of NOP receptors induces antidepressant effects and increases resilience to acute stress. This study investigated the effects of the NOP receptor blockade on dexamethasone-treated mice exposed to acute and prolonged swimming stress. Swiss and NOP(+/+) and NOP(-/-) mice were treated with dexamethasone, and the protective effects of the NOP antagonist SB-612111 (10 mg/kg, ip) or imipramine (20 mg/kg, ip) were investigated in three swimming sessions. The re-exposure to swim stress increased immobility time in Swiss and NOP(+/+), but not in NOP(-/-) mice. Acute and repeated dexamethasone administration induced a further increase in the immobility time, and facilitated body weight loss in Swiss mice. Single administration of SB-612111, but not imipramine, prevented swimming stress- and dexamethasone-induced increase in the immobility time. Repeated administrations of SB-612111 prevented the deleterious effects of 5 days of dexamethasone treatment. Imipramine also partially prevented the effects of re

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