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Dissociative anesthetics, including ketamine and nitrous oxide, impair glutamatergic transmission and mitochondrial function, thereby exacerbating excitotoxicity and neuronal apoptosis

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produced similar neuroendocrine effects in mice than those caused by an acute fast, including suppression of thyroid and reproductive axes, increased glucocorticoid secretion, increase in hypothalamic AgRP and NPY expression and decreased POMC expression 1, 15