Blunted response to low oxygen of rat respiratory network after perinatal ethanol exposure: involvement of inhibitory control

C. Dubois, H. Houchi, M. Naassila, M. Daoust, O. Pierrefiche
The Journal of Physiology. 2008-02-29; 586(5): 1413-1427
DOI: 10.1113/jphysiol.2007.147165

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1. J Physiol. 2008 Mar 1;586(5):1413-27. Epub 2007 Dec 20.

Blunted response to low oxygen of rat respiratory network after perinatal ethanol
exposure: involvement of inhibitory control.

Dubois C(1), Houchi H, Naassila M, Daoust M, Pierrefiche O.

Author information:
(1)Equipe Région INSERM ERI-24 GRAP, Groupe de Recherche sur l’Alcool et
Pharmacodépendances, UFR de Pharmacie, 1, rue des Louvels, 80036 Amiens, France.

Comment in
J Physiol. 2008 Mar 1;586(5):1201.

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 [(3)H]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 microM) demonstrated a higher sensitivity of
expiratory duration in ethanol-exposed animals compared to control animals.
Moreover, [(3)H]strychnine binding density was increased after ethanol and was
associated with higher affinity. Furthermore, 0.2 microM 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.

DOI: 10.1113/jphysiol.2007.147165
PMCID: PMC2375658
PMID: 18096598 [Indexed for MEDLINE]

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