Premature birth, homeostatic plasticity and respiratory consequences of inflammation

Estelle B Gauda1, Gabrielle L McLemore2

  • 1The Hospital for Sick Children, Division of Neonatology, Department of Pediatrics, University of Toronto, Toronto, Ontario, M5G 1X8, Canada.

Insights

Premature birth can disrupt infant respiratory control, leading to breathing issues. This review explores how early birth triggers lasting changes in the respiratory network, increasing risks like apnea and SIDS.

Area of Science:

  • Neonatology
  • Neuroscience
  • Respiratory Physiology

Background:

  • Premature infants face risks like persistent apnea, SIDS, and sleep-disordered breathing.
  • Autonomic nervous system development, crucial for breathing control, occurs late in gestation.
  • Modern neonatology enables survival of extremely premature infants, with significant respiratory system maturation happening outside the womb.

Purpose of the Study:

  • To review the impact of premature birth on respiratory control mechanisms.
  • To explore the concept of homeostatic plasticity in the developing respiratory network.
  • To discuss the link between premature birth, plasticity, and respiratory depression during inflammation.

Main Methods:

  • Literature review focusing on premature birth, autonomic nervous system development, and respiratory control.
  • Analysis of homeostatic plasticity as a mechanism for altered respiratory network output.
  • Discussion of biological pathways involved in respiratory depression in former premature infants.

Main Results:

  • Early birth during the last trimester may induce persistent inhibitory plasticity in the respiratory network.
  • This plasticity can lead to ongoing breathing regulation issues in infancy and childhood.
  • Inflammation can exacerbate respiratory depression in former premature infants due to these altered mechanisms.

Conclusions:

  • Premature birth can fundamentally alter the developing respiratory neural network.
  • Homeostatic plasticity is a key mechanism explaining persistent respiratory dysfunction in ex-utero maturation.
  • Understanding these mechanisms is crucial for managing respiratory risks in premature infants.

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