Fumonisin B1, a toxin produced by Fusarium moniliforme, causes a variety of diseases in animals, including those involving the central nervous system, such as equine leukoencephalomalacia (ELEM). The changes of
biogenic amines may reflect
fumonisin B1 neurotoxicity. It was previously reported that consumption of feed contaminated with Fusarium moniliforme cultures produced an elevation of 5-hydroxyindoleacetic
acid (5-HIAA), the major metabolite of
5-hydroxytryptamine (5-HT), in whole rat brains. In a subsequent study from the same laboratory, rats given
fumonisin B1 orally for 4 weeks showed no changes in
neurotransmitter levels of the whole brain. In the current study, groups of five male BALB/c mice were injected with
fumonisin B1 subcutaneously at doses of 0, 0.25, 0.75, 2.25, 6.75 mg kg-1
body weight daily for 5 days. One day after the last treatment, their brains were dissected into cerebrum, cerebellum, medulla oblongata, midbrain, corpus striatum and hypothalamus. Levels of
norepinephrine (NE),
dopamine (DA), DA metabolites, dihydroxyphenylacetic
acid (
DOPAC) and
homovanillic acid (HVA), and
5-HT and
5-HIAA were determined. A significant elevation of HVA was observed in mice treated with high doses of
fumonisin B1 in most brain regions. In striatum, a decrease of
5-HT was observed by the
fumonisin B1 treatment. Ratios of
neurotransmitters to metabolites such as HVA/DA and 5-HIAA/5-HT were elevated in several brain regions of the treated groups. An accumulation of
neurotransmitter metabolites is suggestive of increased neuronal activity or interference with their efflux from cells.