Exposure to excess glucocorticoid (GC) during early development is implicated in disease risk in later life. GC-induced acceleration of growth-rate leading to adverse phenotypes later is widely observed at the organism level, but cellular and molecular understanding of this process is currently lacking. Using an optogenetic zebrafish model, here we analysed the effects of GC exposure on neurogenesis during development in the whole brain. We identify that the hypothalamus is a highly GC-sensitive region where elevated GC causes precocious development followed by failed maturation and early decline accompanied by impaired feeding, growth, and longevity. In GC-exposed animals, the developmental trajectory of hypothalamic progenitor cells is strikingly altered, potentially mediated by direct regulation of transcription factors such as rx3 by GC. Our data provide cellular and molecular level insight to GC-induced adaptive plasticity leading to allostatic overload in a developing brain, a process crucial for health across the life-course.
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