Alcohol hangover:impairments in behavior and bioenergetics in central nervous system  

作　　者：ANALIA G.KARADAYIAN JUANITA BUSTAMANTE SILVIA LORES-ARNAIZ 

机构地区：[1]Instituto de Bioquímica y Medicina Molecular(IBIMOL)-Universidad de Buenos Aires(UBA),CONICET,Fisicoquímica,Facultad de Farmacia y Bioquímica,Junín 956(C1113AAD),Buenos Aires,Argentina [2]Centro de Altos Estudios en Ciencias Humanas y de la Salud(CAECIHS),Facultad de Medicina,Universidad Abierta Interamericana,Buenos Aires,Argentina

出　　处：《BIOCELL》2016年第1期30-33,共4页生物细胞（英文）

基　　金：supported by grants from Consejo Nacional de Investigaciones Científicas y Técnicas(CONICET,PIP 112-20110100271);Universidad de Buenos Aires(UBA,0020130100255BA),Argentina.

摘　　要：Alcohol hangover(AH)is defined as the temporary state after alcohol binge-like drinking,starting when EtOH is absent in plasma.Results from our laboratory have shown behavioral impairments and mitochon-drial dysfunction in an experimental model of AH in mice.Our model consisted in a single i.p.injection of EtOH(3.8 g/kg BW)or saline solution in male and female mice,sacrificing the animals 6 hours after injection.Motor and affective behavior together with mitochondrial function and free radical production were evaluated in brain cortex and cerebellum during AH.Results showed that hangover animals exhibited a significant reduction in neuromus-cular coordination,motor strength and locomotion together with a loss of gait stability and walking deficiencies.Moreover,an increment in anxiety-like behavior together with fear-related phenotype and depression signs were observed.In relation to bioenergetics metabolism,AH induced a reduction in oxygen uptake,inhibition of respira-tory complexes,changes in mitochondrial membrane permeability,decrease in transmembrane potential,increase in O2•-and H2O2 production and impairment in nitric oxide metabolism.All together our data suggest that the phys-iopathological state of AH involves behavioral impairments and mitochondrial dysfunction in mouse brain cortex and cerebellum showing the long lasting effects of acute EtOH exposure in CNS.

关 键 词：alcohol hangover motor performance ATAXIA mitochondria free radicals 

分 类 号：O62[理学—有机化学]