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Ventilatory long‐term facilitation is altered in tryptophan hydroxylase 2 knock out mice
Author(s) -
Hickner Stephen James,
Angoa-Perez Mariana,
Kuhn Donald M,
Mateika Jason H
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.704.5
Subject(s) - endocrinology , medicine , hypoxia (environmental) , ventilation (architecture) , plethysmograph , carotid body , serotonin , tidal volume , facilitation , hypoxic ventilatory response , chemistry , biology , respiratory system , stimulation , oxygen , receptor , neuroscience , mechanical engineering , organic chemistry , engineering
Purpose This study was designed to examine the impact of serotonin (5HT) in the central nervous system (CNS) on ventilatory long‐term facilitation (vLTF) in spontaneously breathing mice. Methods We exposed six mice with a null mutation for tryptophan hydroxylase 2 (KO) and six wild type mice (WT) to 12 episodes of hypoxia (10 % oxygen) and measured ventilation via whole body plethysmography. ResultsKO WTBaseline V T 0.21 ± 0.03 * 0.17 ± 0.01 Baseline B f 150.5 ± 7.1 * 169.5 ± 6.0 Recovery V T 0.22 ± 0.02 * 0.16 ± 0.01 Recovery B f 152.9± 11.2 * 186.2 ± 4.8 §V T – tidal volume (ml); B f – breathing frequency (breaths/min);* – significantly different from WT mice (p < 0.05);§ – significantly different from baseline (p < 0.05).KO mice displayed an elevated V T and a decreased B f under baseline conditions. LTF was evident in the WT (see B f measures) but not the KO mice following exposure to hypoxia. Conclusions Lack of 5HT in the CNS is accompanied by the absence of LTF following acute exposure to intermittent hypoxia.