Chronic ethanol exposure during the foetal period alters spontaneous neuronal discharge, excitatory and inhibitory amino acid neurotransmission and neuronal sensitivity to ethanol in the adult brain. However, nothing is known about the effects of such exposure on the central respiratory rhythmic network, which is highly dependent on ethanol-sensitive amino acid neurotransmission. In 3- to 4-week-old rats, we investigated: 1) the effects of chronic ethanol exposure during gestation and lactation periods (10% v/v as unique source of fluid) on phrenic (Phr) and hypoglossal (XII) nerve activity using an in situ preparation and on spontaneous breathing at rest in unanaesthetised animals using plethysmography; 2) the sensitivity of the respiratory system to ethanol re-exposure in situ and, 3), phrenic nerve response to muscimol, a GABAA receptor agonist, applied systemically in an in situ preparation. In control rats, ethanol (10-80 mM) induced a concentration-dependent decrease in the amplitude of both XII and Phr motor outflows. At 80 mM ethanol, the two nerves amplitude displayed a difference in their sensitivity to ethanol and respiratory frequency increased due to shortening of post-inspiration. After chronic ethanol exposure, respiratory frequency was significantly reduced by 43% in situ and by 23% in unanaesthetised animals, due to a selective increase in expiratory duration. During Phr burst, the ramp was steeper, revealing modification of inspiratory patterning. Interestingly, re-exposure to ethanol in situ elicited a dramatic inhibitory effect. At 80 mM, ethanol abolished rhythmic XII nerve outflow in all cases and Phr nerve outflow in only 50% of cases. Furthermore, administration of 50 µM muscimol abolished Phr nerve activity in all control rats, but only in 50% of ethanol-exposed animals. Our results demonstrate that chronic ethanol exposure at an early stage of brain development depresses breathing in juvenile rats, and sensitized respiratory network to re-exposure to ethanol which does not seem to involve GABAergic neurotransmission.