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Experimental study demonstrates that glucocorticoid receptor disruption mimics stress-induced locomotor deficits in zebrafish embryos, indicating a critical endocrine pathway in neurodevelopment.
Early life stress produces lasting changes in both neurological and endocrine development that alter later life behavior, stress response, and mental health. Zebrafish have been demonstrated to be useful organisms for studying the effects of early life stress because of their ease of manipulation during the postnatal period, availability of genetic tools, lack of confounding parental care, and well-established behavioral repertoire. The current studies establish a model of early life stress using intermittent light and vibration exposure that creates reductions in baseline locomotion and light/dark transition-induced movement at 4 days post-fertilization. The effects of early life stress on locomotion were mimicked by genetic disruption of the glucocorticoid receptor through a grs357 point mutation and at least partially reversed by pharmacological blockade of cortisol synthesis. In contrast, exogenous hydrocortisone failed to recapitulate the effects of early life stress, but instead increased locomotor behavior, which is consistent with evidence that corticosteroids can alter the rate of locomotor development.
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Burman et al. (2026) studied this question.
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