Journal: Frontiers in Neural Circuits
Article Title: Prostaglandin E2 Exerts Biphasic Dose Response on the PreBötzinger Complex Respiratory-Related Rhythm
doi: 10.3389/fncir.2022.826497
Figure Lengend Snippet: Integrated XII motor output in preBötC slices after exposure to prostanoid receptor agonists. (A) Examples of integrated hypoglossal motor output (XII) of slices exposed to EP2R agonist Butaprost (500 nM), EP3R agonist Sulprostone (1 μM) and non-selective prostanoid receptor agonist 11-deoxy PGE1 (10 nM) (150 s shown per condition). (B) Activating prostanoid receptors with selective agonists modulates burst period of XII motor output. Exposure to EP2R agonist Butaprost decreases burst period (–28% below control, p < 0.01), while EP3R agonist Sulprostone increases burst period (+21% above control, p < 0.0001). Non-selective prostanoid receptor agonist 11-deoxy PGE1 does not change the burst period. (C) EP2R agonist Butaprost decreases average burst amplitude (–35% below control, p < 0.001). (D) EP3R agonist Sulprostone decreases burst width (–9% below control, p < 0.01). (E,F) EP2R agonist Butaprost decreases XII burst area (–44% below control, p < 0.001) and the CV of the burst period (–0.07 below control, p < 0.05) (* p < 0.05, ** p < 0.01, **** p < 0.0001).
Article Snippet: The following drugs were used: EP1 antagonist GW848867X (Cayman Chemicals, Ann Arbor, MI, United States, 50 nM), EP2 Antagonist PF-04418948 (Cayman Chemical, 500 nM), EP3 antagonist DG041 (Tocris, Bristol, United Kingdom, 40 nM), EP4 antagonist MK2894 (APExBIO, Houston, TX, United States, 100 nM), Prostaglandin E2 (Sigma-Aldrich, St. Louis, MO, United States, 1 nM-1 μM), Prostaglandin F receptor antagonist AL-8810 (Cayman Chemical, 1 μM), Prostaglandin D2 receptor antagonist Setipiprant (Cayman Chemical, 500 nM), Non-selective EP2/3/4 agonist 11-deoxy PGE1 (Cayman Chemical, 10 nM), EP2R agonist Butaprost (Cayman Chemical, 5 μM), EP3 receptor agonist Sulprostone (Cayman Chemical, 1 μM).
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