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Prenatal nicotine exposure causes differential impairment of thermogenesis and ventilation in neonatal WT and α4 KO mice
Author(s) -
Avraam Joanne,
Frappell Peter,
Cohen Gary
Publication year - 2011
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.25.1_supplement.1073.2
Subject(s) - nicotine , thermoregulation , endocrinology , medicine , thermogenesis , ventilation (architecture) , chemistry , nicotinic agonist , receptor , obesity , mechanical engineering , engineering
Prenatal nicotine exposure impairs functions necessary for neonatal survival. A mechanism may involve disruption of nicotine acetylcholine receptor‐mediated signalling. We investigated the effects of prenatal nicotine on newborn thermoregulatory and metabolic control, and the role played by α4 subunit‐containing nicotinic acetylcholine receptors (α4 nAChRs) in mediating these effects. Pregnant wild‐type (WT) and α4 nAChR knockout (KO) dams were exposed to nicotine at 6 mg/kg/day from E11 (treated animals). Newborns were studied on day 2 and 7 via open flow respirometry. Pups were exposed to either air or 10% hypoxia whilst ambient temperature (Ta) was lowered from either 30°C or 34°C to 18°C at 0.5°C/min and then re‐raised. Metabolic rate (O 2 consumption and CO 2 production), ventilation (V E ) and body temperature (Tb) were measured continuously. In air, treated WT but not KO pups increased rather than decreased heat production during re‐warming resulting in a higher convective requirement (V E /metabolic rate; ~28.0 versus ~38.5, respectively). During hypoxia the hypometabolic response of both genotypes remained intact, although hypoxic hyperpnea was attenuated by different mechanisms (V T in WT, V T and F B in KO pups). The results indicate that α4 nAChRs are involved in the control of thermoregulation and ventilation and provide evidence suggesting an inhibitory role that can be altered by nicotine.