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Heart rate control, but not the ventilatory response to CO2, is altered in 5HT 1A receptor knock‐out (KO) mice during early development: possible relevance for Sudden Infant Death Syndrome (SIDS)
Author(s) -
Barrett Karlene,
Daubenspeck Andrew,
Li Aihua,
Nattie Eugene
Publication year - 2010
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.24.1_supplement.623.8
Subject(s) - sudden infant death syndrome , 5 ht receptor , medicine , endocrinology , receptor , serotonin , pathogenesis , biology , pediatrics
Abnormalities in the medullary serotonin (5HT) system, including a decrease in the 5HT 1A receptor binding density, have been implicated in the sudden infant death syndrome (SIDS), but it is uncertain how such abnormalities translate into a mechanism for its pathogenesis. Using the 5HT 1A receptor KO mouse as a model of a system with reduced 5HT 1A activity, we studied breathing, heart rate and the occurrence of spontaneous bradycardias in KO and control mice of both genders in air and in response to 5% CO 2 at postnatal days (P) 5, 15 and 25. Breathing, represented as V E /V O2 , was unaffected by the absence of the 5HT 1A receptor both in air and in response to 5% CO 2 at all ages studied, and in both genders, except in the P15 heterozygous males, that had a 42% reduction in the V E /V O2 in air. Heart rate was significantly reduced at P5 in females in air and CO 2 , and in P15 males in air. P15 and P25 KO male pups had 6 and 7.5 – fold more spontaneous bradycardias, respectively in air, and time and frequency domain analyses of the R‐R intervals at these two ages showed greater variability in the KO pups compared to controls during CO 2 . These data suggest that heart rate control during early development is adversely affected in mice lacking the 5HT 1A receptor. (HD036379; 5HT 1A KO mice were generously supplied by R. Hen)