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Prostaglandin E2 Exerts Biphasic Dose Response on the PreBötzinger Complex Respiratory-Related Rhythm

Jan Philipp Reising1,2, Wiktor S Phillips1,2, Naify Ramadan1,2

  • 1Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.

Frontiers in Neural Circuits
|June 7, 2022
PubMed

Insights

Prostaglandin E2 (PGE2) affects infant breathing by altering inspiratory motor rhythm. This study reveals how PGE2, acting on EP2 and EP3 receptors, influences breathing patterns in response to inflammation.

Area of Science:

  • Neuroscience
  • Respiratory Physiology
  • Molecular Biology

Background:

  • Infant inflammation can lead to life-threatening respiratory dysfunction.
  • Prostaglandin E2 (PGE2), released during inflammation, is known to disrupt breathing patterns.
  • The preBötzinger complex (preBötC) is crucial for generating the respiratory rhythm.

Purpose of the Study:

  • To investigate the concentration-dependent effects of PGE2 on the inspiratory motor rhythm generated by the preBötC.
  • To identify the specific prostanoid receptors (EP1-4R, FPR, DP2R) involved in mediating PGE2's effects on breathing.
  • To explore the cellular localization of EP2 and EP3 receptors within the preBötC.

Main Methods:

  • Utilized rhythmic medullary slice preparations to measure motor output.
  • Administered varying concentrations of PGE2 (1 nM-1 μM) to assess dose-dependent effects.
  • Employed specific pharmacology targeting prostanoid receptors and analyzed single-cell RNA-Seq data.

Main Results:

  • Low PGE2 concentrations (1-10 nM) increased inspiratory burst period duration; high concentrations (1 μM) decreased it.
  • Coactivation of EP2 and EP3 receptors was necessary for PGE2 to modulate the inspiratory burst period.
  • EP2 receptor transcripts were found in excitatory neurons, while EP3 receptor transcripts were in inhibitory neurons within the preBötC.

Conclusions:

  • PGE2 exerts a biphasic concentration-dependent effect on inspiratory motor rhythm via EP2 and EP3 receptors.
  • The differential expression of EP2 and EP3 receptors in distinct neuronal populations contributes to the observed effects.
  • Understanding these mechanisms is vital for addressing inflammatory-induced respiratory dysfunction in infants.

Keywords:
inflammationneural networkspreBötzinger complex (preBötC)prostaglandin E2 (PGE2)respiratory – mechanics

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