HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 586/5/1413    most recent jphysiol.2007.147165v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Dubois, C. Articles by Pierrefiche, O. PubMed PubMed Citation Articles by Dubois, C. Articles by Pierrefiche, O. Related Collections Respiratory Related Article

¹ Equipe Région INSERM ERI-24 GRAP, Groupe de Recherche sur l'Alcool et les Pharmacodépendances, Faculté de Pharmacie, 1 rue des Louvels, F-80036 Amiens, France

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- and postnatal ethanol exposure induced low minute ventilation in juvenile rats. The present study analysed in juvenile rats the respiratory response to hypoxia in vivo by plethysmography and the phrenic (Phr) nerve response to ischaemia in situ. Glycinergic neurotransmission was assessed in situ with strychnine application and [³H]strychnine binding experiments performed in the medulla. After chronic ethanol exposure, hyperventilation during hypoxia was blunted in vivo. In situ Phr nerve response to ischaemia was also impaired, while gasping activity occurred earlier and recovery was delayed. Strychnine applications in situ (0.05–0.5 µM) demonstrated a higher sensitivity of expiratory duration in ethanol-exposed animals compared to control animals. Moreover, [³H]strychnine binding density was increased after ethanol and was associated with higher affinity. Furthermore, 0.2 µM strychnine in ethanol-exposed 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.

(Received 23 October 2007; accepted after revision 18 December 2007; first published online 20 December 2007)
Corresponding author O. Pierrefiche: Equipe Région INSERM ERI-24 GRAP, Groupe de Recherche sur l'Alcool et les Pharmacodépendances, UFR de Pharmacie, 1, rue des Louvels, 80036 Amiens, France. Email: op-lnc{at}u-picardie.fr

Related Article

Maternal drinking of alcohol: the newborn has the worst hangover

Walter M. St.-John
J. Physiol. 2008 586: 1201. [Full Text] [PDF]

This article has been cited by other articles:

				W. M. St.-John Maternal drinking of alcohol: the newborn has the worst hangover J. Physiol., March 1, 2008; 586(5): 1201 - 1201. [Full Text] [PDF]