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Autoresuscitation responses to hypoxia‐induced apnea are prolonged in newborn 5HT‐deficient Pet‐1 homozygous mice
Author(s) -
Erickson Jeffery T,
Sposato Brian C,
Mecker Samantha V
Publication year - 2009
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.23.1_supplement.961.1
Subject(s) - hypoxia (environmental) , apnea , 5 ht receptor , knockout mouse , period (music) , endocrinology , medicine , serotonin , biology , chemistry , oxygen , receptor , physics , organic chemistry , acoustics
Autoresuscitation is a critical survival‐promoting mechanism in mammals that allows recovery from primary apnea via hypoxia‐induced gasping. Serotonin (5HT) neurotransmission has been implicated in gasp generation and autoresuscitation although the role of endogenous 5HT in these processes in vivo is not yet clear. In this study we used body plethysmography to compare autoresuscitation responses to hypoxia‐induced apnea in unanesthetized newborn wild type (WT) mice and Pet‐1 knockout (KO) mice that have only 30% of the normal complement of brainstem 5HT neurons. When exposed to 97% N 2 /3% CO 2 on postnatal day 4.5, the time to first gasp following primary apnea was significantly longer in the KO compared to WT mice. During unrelenting hypoxia the gasp frequency, the total number of gasps generated, the duration of the gasping period, and the time to last gasp was similar between genotypes. However, if O 2 was made available before the first gasp, allowing for autoresuscitation to occur, gasping frequency was decreased and the duration of the gasping period was prolonged in KO mice, relative to the WT, resulting in a significant increase in the time needed for a successful autoresuscitation response. We conclude that 5HT‐deficient Pet‐1 KO mice can gasp and autoresuscitate from a single episode of hypoxia‐induced apnea, but autoresuscitation is inefficient, relative to WT controls. Supported by a TCNJ SOSA award (JTE).