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Effects of pharmacologic manipulation of the brainstem serotonergic system on duration of the laryngeal chemoreflex—implications for Sudden Infant Death Syndrome
Author(s) -
Donnelly William Thomas,
Bartlett Donald,
Leiter James C.
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.1090.3
Subject(s) - sudden infant death syndrome , serotonergic , apnea , serotonin , medicine , anesthesia , ketanserin , brainstem , 5 ht receptor , antagonist , endocrinology , receptor , pediatrics
Sudden infant death syndrome (SIDS) occurs when a sleeping infant fails to mount an effective response to a challenge to cardiorespiratory homeostasis. Serotonin receptor binding in the nucleus of the solitary tract (NTS) is reduced in infants who die of SIDS. The laryngeal chemoreflex (LCR) causes apnea and may initiate the process leading to SIDS. We tested the hypothesis that altering serotonergic signaling in the NTS would alter the duration of LCR apnea. Rat pups (P5 to P20) were anesthetized and tracheostomized. Tracheal tubing was inserted rostrally up to the larynx, and water was instilled to elicit the LCR. The EKG and intercostal EMG activity were recorded. ICV serotonin shortened apnea duration, and ICV WAY100635 (a 5HT‐1A receptor antagonist) prolonged it. ICV ketanserin (a 5HT‐2A receptor antagonist) had no consistent effect on apnea duration. Focal injection of WAY100635 in the cNTS also had no consistent effect on apnea duration, but injection of serotonin in this area shortened it. We conclude that serotonin within the NTS shortens the duration of LCR apnea, but this effect cannot be attributed solely to activation of 5HT‐1A receptors. Support: NIH grants HL36379 & HL42707