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The Journal of Neuroscience, December 17, 2008, 28(51):13907-13917; doi:10.1523/JNEUROSCI.4441-08.2008

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Neurobiology of Disease
Prenatal to Early Postnatal Nicotine Exposure Impairs Central Chemoreception and Modifies Breathing Pattern in Mouse Neonates: A Probable Link to Sudden Infant Death Syndrome

Jaime Eugenín,¹ Marcelo Otárola,¹ Eduardo Bravo,¹ Claudio Coddou,¹ Verónica Cerpa,¹ Miguel Reyes-Parada,^2,3 Isabel Llona,¹ and Rommy von Bernhardi⁴

¹Laboratory of Neural Systems, Department of Biology, Faculty of Chemistry and Biology, and ²Faculty of Medical Sciences, Universidad de Santiago de Chile (USACH), Santiago 9160000, Chile, ³Millenium Institute for Cell Dynamics and Biotechnology, Santiago 8370456, Chile, and ⁴Laboratory of Neuroscience, Department of Neurology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile

Correspondence should be addressed to Dr. Jaime Eugenín, Laboratory of Neural Systems, Department of Biology, Faculty of Chemistry and Biology, Universidad de Santiago de Chile, USACH, Casilla 40, Correo 33, Santiago 1, Santiago 9160000, Chile. Email: jaime.eugenin{at}usach.cl or Email: jeugenin{at}gmail.com

Nicotine is a neuroteratogen and is the likely link between maternal cigarette smoking during pregnancy and sudden infant death syndrome (SIDS). Osmotic minipumps were implanted in 5–7 d CF1 pregnant mice to deliver nicotine bitartrate (60 mg Kg^–1 day^–1) or saline (control) solutions for up to 28 d. Prenatal to early postnatal nicotine exposure did not modify the number of newborns per litter or their postnatal growth; however, nicotine-exposed neonates hypoventilated and had reduced responses to hypercarbia (inhalation of air enriched with 10% CO₂ for 20 min) and hypoxia (inhalation of 100% N₂ for 20 s) at postnatal days 0–3 (P0–P3). In contrast, at postnatal day 8, nicotine-exposed neonates were indistinguishable from controls. Isolated brainstem–spinal cord preparations obtained from P0 to P3 nicotine-exposed neonates showed fictive respiration with respiratory cycles longer and more irregular than those of controls, as indicated by high short- and long-term variability in Poincaré plots. In addition, their responses to acidification were reduced, indicating compromise of central chemoreception. Furthermore, the cholinergic contribution to central chemosensory responses switched from muscarinic receptor to nicotinic receptor-based mechanisms. No significant astrogliosis was detectable in the ventral respiratory group of neurons with glial fibrillary acidic protein immunohistochemistry. These results indicate that nicotine exposure affects the respiratory rhythm pattern generator and causes a decline in central chemoreception during early postnatal life. Consequently, breathing would become highly vulnerable, failing to respond to chemosensory demands. Such impairment could be related to the ventilatory abnormalities observed in SIDS.

Key words: nicotine; central chemoreception; respiratory rhythm generator; sudden infant death syndrome; hypercarbia; hypoxia; acetylcholine

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Received Sept. 17, 2008; revised Oct. 23, 2008; accepted Oct. 29, 2008.

Correspondence should be addressed to Dr. Jaime Eugenín, Laboratory of Neural Systems, Department of Biology, Faculty of Chemistry and Biology, Universidad de Santiago de Chile, USACH, Casilla 40, Correo 33, Santiago 1, Santiago 9160000, Chile. Email: jaime.eugenin{at}usach.cl or Email: jeugenin{at}gmail.com

This article has been cited by other articles:

				K. J. Muller, G. Tsechpenakis, R. Homma, J. G. Nicholls, L. B. Cohen, and J. Eugenin Optical analysis of circuitry for respiratory rhythm in isolated brainstem of foetal mice Phil Trans R Soc B, September 12, 2009; 364(1529): 2485 - 2491. [Abstract] [Full Text] [PDF]

				C. Coddou, E. Bravo, and J. Eugenin Alterations in cholinergic sensitivity of respiratory neurons induced by pre-natal nicotine: a mechanism for respiratory dysfunction in neonatal mice Phil Trans R Soc B, September 12, 2009; 364(1529): 2527 - 2535. [Abstract] [Full Text] [PDF]

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