A novel, translational mouse model of prenatal methadone exposure was developed and a longitudinal assessment of offspring revealed impairments in physical, behavioral, and neuronal development.

Vocal development in marmoset monkeys begins in utero.

Mice deficient in the TRPM6 channel suffer from impaired prenatal development, shortened lifespan, growth deficit and disturbed energy balance due to a defect in epithelial Mg²⁺ uptake, thus highlighting a pivotal role of TRPM6 in organismal Mg²⁺ homeostasis.

Pacemaker neurons are present in the preBötC circuitry of mouse embryos and their role in driving respiratory network activity changes during the critical period immediately before birth.

Loss miRNA maturation in proopiomelanocortin (POMC) neurons causes metabolic dysregulation and favors the differentiation of Pomc progenitors into neuropeptide Y neurons, a developmental process that appears to specifically involve miR-103/107.

Foxp2 is dispensable for several features of cortical development that were previously considered to depend on its function.

Prenatal stress is transmitted to infant development through cortisol, which imparts sex-specific effects on the development and connectivity of the amygdalae.

A nonlinear deep generative model can represent fetal–neonatal resting-state functional magnetic resonance imaging better than conventional linear models.

A useful single-cell resource provides the prenatal macaque different cell types’ gene expression profiles in the parietal cerebral cortex lobe.

Functional and anatomical analysis reveal a crucial role played during embryonic development by microglia in the ontogenesis and function of central circuits responsible for respiratory rhythmogenesis.