Some female insects exhibit a drastic suppression of egg production under unfavourable environmental conditions, such as low temperatures, which is referred to as reproductive dormancy. This state appears to be partly mediated by signals from the brain that induce the corpus allatum (CA) to downregulate juvenile hormone (JH) production. However, little is known about this connection between the CA and the brain. Working in Drosophila, Ryusuke Niwa and colleagues use immunostaining to identify that neurons projecting from the brain to the CA express the diuretic hormone 31 (DH31) neuropeptide. They find that stimulating these neurons is sufficient to suppress oogenesis. By contrast, depleting Dh31 under dormancy-inducing conditions results in enlarged ovaries and greater oocyte production. The authors obtain a similar phenotype when they knock down the gene encoding the DH31 receptor (DH31-R), which is expressed in the CA. Loss of Dh31 or Dh31-R also results in higher levels of circulating JH. DH31-R acts through cAMP and the authors show that the application of synthetic DH31 ex vivo drives higher intracellular cAMP levels in the CA cells in a DH31-R-dependent manner. Together, this work identifies peptidergic neurons connecting the CA and brain that play a role in initiating reproductive dormancy via JH suppression.