Early ethanol exposure alters neonatal breathing plasticity. Respiratory EtOH's effects are attributed to central respiratory network disruptions, particularly in the medullary serotonin (5HT) system. In this study we evaluated the effects of neonatal pre-exposure to low/moderate doses upon breathing rates, activation patterns of brainstem’s nuclei and expression of 5HT 2A and 2C receptors. At PD9, breathing frequencies, tidal volumes and apneas were examined in pups pre-exposed to vehicle or ethanol (2.0 g/kg) at PDs 3, 5 and 7. This developmental stage is equivalent to the 3^rd human gestational trimester, characterized by increased levels of synaptogenesis. Pups were tested under sobriety or under the state of ethanol intoxication and when subjected to normoxia or hypoxia. Number of c-Fos and 5HT immunolabelled cells and relative mRNA expression of 5HT 2A and 2C receptors were quantified in the brainstem. Under normoxia, ethanol pre-exposed pups exhibited breathing depressions and a high number of apneas. An opposite phenomenon was found in ethanol pre-treated pups tested under hypoxia where an exacerbated hypoxic ventilatory response (HVR) was observed. The breathing depression was associated with an increase in the neural activation levels of the raphe obscurus (ROb) and a high mRNA expression of the 5HT 2A receptor in the brainstem while desactivation of the ROb and high activation levels in the solitary tract nucleus and area postrema were associated to the exacerbated HVR. In summary, early ethanol experience induces respiratory disruptions indicative of sensitization processes. Neuroadaptive changes in central respiratory areas under consideration appear to be strongly associated with changes in their respiratory plasticity.

早期乙醇暴露改变新生儿呼吸可塑性。呼吸乙醇的影响归因于中枢呼吸网络中断，特别是在髓质血清素 (5HT) 系统中。在这项研究中，我们评估了新生儿预先暴露于低/中剂量对呼吸频率、脑干核的激活模式和 5HT 2A 和 2C 受体表达的影响。在PD9，呼吸频率，潮气量和呼吸暂停是在幼鼠预暴露于车辆或乙醇（2.0克/公斤）的PD 3,5和7。该发育阶段是相当于3检查^RD人类妊娠三个月，其特点是突触发生水平增加。幼崽在清醒或乙醇中毒状态下以及在常氧或缺氧条件下进行测试。在脑干中量化 c-Fos 和 5HT 免疫标记细胞的数量以及 5HT 2A 和 2C 受体的相对 mRNA 表达。在常氧条件下，预先暴露于乙醇的幼崽表现出呼吸抑制和大量呼吸暂停。在缺氧条件下测试的乙醇预处理幼崽中发现了相反的现象，其中观察到缺氧通气反应 (HVR) 加剧。呼吸抑制与暗中缝 (ROb) 神经激活水平的增加和脑干中 5HT 2A 受体的高 mRNA 表达有关，同时 ROb 的失活和孤立束核和后区的高激活水平与加重的 HVR 相关。总之，早期的乙醇经验会导致呼吸中断，表明敏化过程。所考虑的中央呼吸区的神经适应性变化似乎与其呼吸可塑性的变化密切相关。