Fumonisin B1 facilitates seizures induced by pentylenetetrazol in mice

• FB1 decreased the latency to myoclonic jerks induced by PTZ.
• FB1 facilitated the development of seizures induced by PTZ.
• FB1 exposure increased the ΔΨm in the cerebral cortex.
• FB1 exposure increased total and α1 Na+,K+-ATPase activities in the cerebral cortex.
• Acute exposure to FB1 causes brain hyperexcitability in vivo.

Fumonisin B1 (FB1) is a Fusarium spp. mycotoxin which constitutes a major public health issue because of its worldwide distribution and diversity of toxic effects. While the liver and kidney are considered the major target organs of FB1 toxicity in several species, evidence indicates that FB1 may be toxic to the brain. To further investigate the effects of FB1 on the central nervous system the present study aimed to test the hypothesis that acute FB1 exposure causes brain hyperexcitability and the potential underlying mechanisms. For these purposes, adult male C57BL/6 mice were injected with FB1 (8 mg/kg, i.p.) or its vehicle and 30 min thereafter received with a low dose of the classical convulsant pentylenetetrazol (PTZ, 30 mg/kg, i.p.) or its vehicle. After behavioral evaluation the cerebral cortex and the hippocampus were collected for analysis of Na+,K+-ATPase activity, mitochondrial membrane potential (ΔΨm) and mitochondrial complex I and II activities. We found that FB1 reduced the latency for PTZ-induced myoclonic jerks and increased the number of these events. After exposure to FB1 total and α1 Na+,K+-ATPase activities increased in cerebral cortex, whereas the same enzyme activities decreased in the hippocampus. Although no changes in mitochondrial complex I and II activities were found, acute exposure to FB1 increased ΔΨm in the cerebral cortex. Altogether, present results indicate that FB1 causes brain hyperexcitability in vivo, and that mitochondrial dysfunction may represent a potential underlying mechanism.