Acetaldehyde-induced alterations in metabolism of monoamines in mouse brain

The effects of single and repeated inhalations of acetaldehyde (AcAl) on spontaneous activity and the metabolisms of cerebral monoamines and neuroactive amino acids were investigated. Both single and repeated inhalations of AcAl induced a significant increase of spontaneous activity at the initial stage followed by the loss of motor activity and coma. The AcAl inhalation-induced central excitement, exhibited by hyperkinesia and occasional jumpings, were found to be more severe following a single administration than by repeated ones. These abnormal behaviors observed following a single administration of AcAl, were accompanied by significant decreases of noradrenaline in the cerebral cortex, brainstem and of dopamine in the brainstem. In addition, it was found that these decreases in catecholamines were associated with significant decreases in the contents of 3-methoxy-4-hydroxyphenylethyleneglycol, 3, 4-dihydroxyphenylacetic acid and homovanillic acid in brain. The contents of aspartic acid in the cerebral cortex and of GABA in the brainstem also showed an increase. On the other hand, animals subjected to the repeated inhalation of AcAl and exhibiting a state of central depression, showed the increase of adrenaline as well as the decrease of GABA in the cerebellum. These results suggest that a single inhalation of AcAl may induce central excitation as well as facilitate the metabolic turnover of cerebral catecholamines, while repeated inhalation of AcAl may result in central depression accompanied by decreased turnover of central catecholamines. Possible involvement of the changes in cerebral aspartic acid and GABA in the exhibition of central effects of AcAl is also suggested.