Open Access

ARTICLE

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

Analia G. Karadayian¹, Juanita Bustamante², Silvia Lores-Arnaiz^{1, *}

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.

* Address correspondence to: Silvia Lores-Arnaiz,

BIOCELL 2016, 40(1), 31-34. https://doi.org/10.32604/biocell.2016.40.031

Abstract

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 mitochondrial 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 neuromuscular 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 respiratory 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 physiopathological 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.

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