Pet1 neurons actively maintain cardiorespiratory tone and dynamic range in mouse neonates and critically support the recovery response to apneas, informing brain findings in the sudden infant death syndrome.

A single neonatal inflammatory event induces long-term impairments in two forms of adult respiratory motor plasticity, an important aspect of the control of breathing for compensation after injury or disease.

Age-specific transcriptional responses to Flt3-ITD and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult, but not fetal/neonatal, stages of development.

Atoh1 promotes the development of two different neural circuits involved in hypoxic and hypercapnic respiratory responses that together are essential for neonatal respiratory drive and survival.

Combined optogenetics and electrophysiology in vivo identified the cellular substrate of hippocampal drive that initiates the oscillatory entrainment of prefrontal cortex in neonatal mice.

Single-cell RNA sequencing of neonatal uterus revealed an Misr2+ endometrial stromal progenitor whose inhibition by ectopic administration of MIS caused uterine hypoplasia and infertility in adulthood.

Motoneuron activity provides feedback to the spinal network responsible for generating locomotion in the developing mouse spinal cord.

Compliant matrix provides a permissive micoenvironment for cardiomyocyte dedifferentiation, cell division and expansion, and thus may open a new avenue towards cardiac regeneration.

Mutations causing proinsulin misfolding trigger unfolded protein response and lead to impaired proliferation and reduced mTORC1 signalling of developing beta-cells in a patient-derived induced pluripotent stem cell disease model.

The pain mediator bradykinin was found to sensitize spinal motoneurons by a direct postsynaptic action, questioning the role of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is commonly used as a surrogate pain model.