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Postnatal loss of brainstem serotonin neurones compromises the ability of neonatal rats to survive episodic severe hypoxia
Author(s) -
Cummings Kevin J.,
Hewitt Julie C.,
Li Aihua,
Daubenspeck John A.,
Nattie Eugene E.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.214445
Subject(s) - hypoxia (environmental) , brainstem , bradycardia , serotonin , endocrinology , medicine , heart rate , sudden infant death syndrome , anesthesia , chemistry , receptor , blood pressure , oxygen , organic chemistry , pediatrics
Non‐Technical Summary Failure to withstand severe hypoxia (failed autoresuscitation) has been documented in sudden infant death syndrome (SIDS) cases, and SIDS is associated with a constellation of defects within the brainstem serotonin system, including reduced serotonin content. Neonatal mice with reduced numbers of serotonergic neurones beginning in utero also have major defects in autoresuscitation at the beginning of the second postnatal week. Here we injected a neurotoxin into the brainstems of 2‐ to 3‐day‐old rat pups, reducing serotonin content by ∼80%, and at P7–10 tested their ability to autoresuscitate when challenged with repeated episodes of environmental anoxia. Pups with reduced serotonin content have delayed gasping in response to each challenge, as well as a significantly higher mortality by the last episode. These new data imply that a postnatal loss of brainstem serotonin in infants could increase the risk of SIDS during severely hypoxic conditions.