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1 Physiology, Dartmouth Medical School, Lebanon, New Hampshire, United States
2 Lebanon, New Hampshire, United States; Physiology, Dartmouth Medical School, Lebanon, New Hampshire, United States
3 Department of Cellular and Molecular, Yale School of Medicine, New Haven, Connecticut, United States
4 Pathology, Children's Hospital Boston, Boston, Massachusetts, United States
* To whom correspondence should be addressed. E-mail: eliana.m.penatti{at}dartmouth.edu.
Acute inhibition of serotonergic (5-HT) neurons in the medullary raphe (MR) using a 5-HT1A receptor agonist had an age-dependent impact on the CO2 response of piglets (33). Our present study explored the effect of chronic 5-HT neuron lesions in the MR and extra-raphe (ER) on the ventilatory response to hypercapnia and hypoxia in piglets with possible implications on the role of 5-HT in the Sudden Infant Death Syndrome (SIDS). We established four experimental groups. Group 1 (n=11) did not undergo any treatment. Groups 2, 3 and 4 were injected with either vehicle or the neurotoxin 5, 7-dihydroxytryptamine (DHT) in the cisterna magna during the first week of life (Group 2, n=9; Group 4, n=11) or second week of life (Group 3, n=10). Ventilation was recorded in response to 5% CO2 (all groups) and 12% O2 (Group 2) during wakefulness and sleep up to postnatal day 25. Surprisingly, the piglets did not reveal changes in their CO2 sensitivity during early postnatal development. Overall, considerable lesions of 5-HT neurons (up to 65% decrease) in the MR and ER had no impact on the CO2 response, regardless of injection time. Post-lesion raphe plasticity could explain why we observed no effect. DHT treated males, however, did present a lower CO2 response during sleep. Hypoxia significantly altered the frequency (fR) during sleep in lesioned piglets. Further studies are necessary to elucidate the role of plasticity, gender and 5-HT abnormalities in SIDS.
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