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Blunted response to low oxygen of rat respiratory network after perinatal ethanol exposure: involvement of inhibitory
C Dubois1, H Houchi, M Naassila
1Equipe Région INSERM ERI-24 GRAP, Groupe de Recherche sur l'Alcool et Pharmacodépendances, UFR de Pharmacie, 1, rue des Louvels, 80036 Amiens, France.
Insights
Chronic ethanol exposure in developing rats impairs respiratory responses to low oxygen by increasing inhibitory neurotransmission. This can be a risk factor for newborns adapting to oxygen-deprived environments.
Area of Science:
- Neuroscience
- Respiratory Physiology
- Developmental Toxicology
Background:
- Chronic ethanol exposure during gestation and early development has known detrimental effects on central nervous system (CNS) development.
- Previous research indicated that prenatal and postnatal ethanol exposure leads to reduced minute ventilation in juvenile rats.
Purpose of the Study:
- To investigate the respiratory response to hypoxia in juvenile rats following chronic ethanol exposure.
- To assess the impact of ethanol on phrenic nerve activity and glycinergic neurotransmission in the medulla.
Main Methods:
- In vivo plethysmography to measure respiratory response to hypoxia.
- In situ assessment of phrenic nerve activity during ischemia.
- Strychnine application and [(3)H]strychnine binding experiments to evaluate glycinergic neurotransmission.
Main Results:
- Ethanol-exposed rats exhibited blunted hyperventilation during hypoxia and impaired phrenic nerve response to ischemia.
- Increased sensitivity to strychnine and higher [(3)H]strychnine binding density indicated enhanced central glycinergic inhibition.
- Polycythemia was observed in ethanol-exposed rats, potentially compensating for reduced resting ventilation.
Conclusions:
- Chronic ethanol exposure during development increases central glycinergic tonic inhibition, impairing the respiratory network's adaptive response to hypoxia.
- Ethanol exposure may pose a risk to neonatal respiratory adaptation in low-oxygen conditions.
- Gasping mechanisms were not affected, but recovery from ischemia was delayed.
Abstract:
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.
