{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:26:56Z","timestamp":1791224816829,"version":"4.1.0"},"reference-count":54,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2008,2,29]],"date-time":"2008-02-29T00:00:00Z","timestamp":1204243200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:p>Acute ethanol depresses respiration, but little is known about chronic ethanol exposure during gestation and breathing, while the deleterious effects of ethanol on CNS development have been clearly described. In a recent study we demonstrated that pre\u2010 and postnatal ethanol exposure induced low minute ventilation in juvenile rats. The present study analysed in juvenile rats the respiratory response to hypoxia<jats:italic>in vivo<\/jats:italic>by plethysmography and the phrenic (Phr) nerve response to ischaemia<jats:italic>in situ<\/jats:italic>. Glycinergic neurotransmission was assessed<jats:italic>in situ<\/jats:italic>with strychnine application and [<jats:sup>3<\/jats:sup>H]strychnine binding experiments performed in the medulla. After chronic ethanol exposure, hyperventilation during hypoxia was blunted<jats:italic>in vivo<\/jats:italic>.<jats:italic>In situ<\/jats:italic>Phr nerve response to ischaemia was also impaired, while gasping activity occurred earlier and recovery was delayed. Strychnine applications<jats:italic>in situ<\/jats:italic>(0.05\u20130.5 \u03bc<jats:sc>m<\/jats:sc>) demonstrated a higher sensitivity of expiratory duration in ethanol\u2010exposed animals compared to control animals. Moreover, [<jats:sup>3<\/jats:sup>H]strychnine binding density was increased after ethanol and was associated with higher affinity. Furthermore, 0.2 \u03bc<jats:sc>m<\/jats:sc>strychnine in ethanol\u2010exposed animals restored the low basal Phr nerve frequency, but also the Phr nerve response to ischaemia and the time to recovery, while gasping activity appeared even earlier with a higher frequency. Polycythaemia was present after ethanol exposure whereas lung and heart weights were not altered. We conclude that chronic ethanol exposure during rat brain development (i) induced polycythaemia to compensate for low minute ventilation at rest; (ii) impaired the respiratory network adaptive response to low oxygen because of an increase in central glycinergic tonic inhibitions, and (iii) did not affect gasping mechanisms. We suggest that ethanol exposure during early life can be a risk factor for the newborn respiratory adaptive mechanisms to a low oxygen environment.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.147165","type":"journal-article","created":{"date-parts":[[2007,12,21]],"date-time":"2007-12-21T01:58:29Z","timestamp":1198202309000},"page":"1413-1427","source":"Crossref","is-referenced-by-count":28,"title":["Blunted response to low oxygen of rat respiratory network after perinatal ethanol exposure: involvement of inhibitory 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