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Brainstem Serotonergic Deficiency in Sudden Infant Death Syndrome
Author(s) -
Jhodie R. Duncan
Publication year - 2010
Publication title -
jama
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.688
H-Index - 680
eISSN - 1538-3598
pISSN - 0098-7484
DOI - 10.1001/jama.2010.45
Subject(s) - sudden infant death syndrome , tph2 , medicine , serotonergic , serotonin , endocrinology , sudden death , tryptophan hydroxylase , raphe , dorsal raphe nucleus , apnea , brainstem , receptor , pediatrics
Sudden infant death syndrome (SIDS) is postulated to result from abnormalities in brainstem control of autonomic function and breathing during a critical developmental period. Abnormalities of serotonin (5-hydroxytryptamine [5-HT]) receptor binding in regions of the medulla oblongata involved in this control have been reported in infants dying from SIDS.

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