Ethanol consumption is correlated with different neurobiological and behavioral impairments. Acute and chronic exposure to this drug is associated with alterations in the regulation of the mesolimbic dopaminergic system as well as with transcriptional modulation of other receptors in the central nervous system and can unleash seeking behavior or behavioral adaptations and phenotypes such as loss of control, dependence and tolerance. In the present work, we characterized the chronological effects of acute and chronic intermittent exposure to ethanol (1% v/v) in an adult zebrafish population (Danio rerio). During sixteen days of ethanol exposure, we associated the neuromodulation of target genes (drd1, drd2, gabra2a, gabbr1a, gabbr1b) in the central nervous system with behavioral parameters, assessed by social preference, antipredatory capacity and anxiety-like analysis. Transcriptional and behavioral data were collected in days 0, 1, 4, 8, 12 and 16, after ethanol exposure. In days 1 and 4, ethanol exposure increased exploratory behavior regardless of the risk involved (less time spent close to conspecifics and lower avoidance reaction to predator). Along with the reduction of drd2, grin1a and gabra2a transcription seen in the same days, these results suggest an anxiolytic effect of acute ethanol exposure. Interestingly, in days 8, 12 and 16, an attenuation of the behavioral effects was observed. The social preference, antipredatory behavior, perception and exploration parameters were reconstituted. This behavioral re-establishment, accompanied by the increase in drd1, drd2 and gabbr1a transcription in the 8th day could be an indicative of an adaptation to chronic exposure to ethanol. The modulation of drd2 gene combined with the behavioral characterization observed in the study suggests this signalling pathway as a key participant in the phenotypic outcomes of a long-term chronic exposure to ethanol. Lastly, our results reaffirm the ethanol deleterious impacts in perception, ability to respond to adverse stimuli and in anxiety-like behavior.

乙醇消耗与不同的神经生物学和行为障碍相关。急性和长期暴露于这种药物与中脑边缘多巴胺能系统的调节改变以及中枢神经系统中其他受体的转录调节有关，并且可以释放寻求行为或行为适应性和表型，例如失去控制，依赖性和宽容。在目前的工作中，我们表征了成年斑马鱼种群（Danio rerio）急性和慢性间歇性暴露于乙醇（1％v / v）的时间顺序影响。在乙醇暴露的16天中，我们关联了靶基因（drd1，drd2，gabra2a，（gabbr1a，gabbr1b）在中枢神经系统中的行为参数，通过社交偏好，抗掠食能力和焦虑样分析进行评估。在暴露于乙醇后的第0、1、4、8、12和16天收集了转录和行为数据。在第1和第4天，乙醇暴露增加了探索行为，无论涉及到什么风险（花费更少的时间接近特定物种，并且减少了对捕食者的反应）。随着drd2，grin1a和gabra2a的减少在同一天看到转录，这些结果表明急性乙醇暴露具有抗焦虑作用。有趣的是，在第8、12和16天观察到了行为影响的减弱。重构了社会偏好，反掠夺行为，知觉和探索参数。这种行为的重新建立，伴随着第8天drd1，drd2和gabbr1a转录的增加，可能表明适应了慢性暴露于乙醇。drd2的调制该基因与研究中观察到的行为特征相结合，表明该信号通路是长期长期暴露于乙醇的表型结果的关键参与者。最后，我们的结果再次证实了乙醇对感知，对不良刺激的反应能力以及焦虑样行为的有害影响。