Mitochondrial toxins represent an interesting group of neurotoxicants related both to causation and modelling of central nervous damage. 3-nitropropionic acid (3NP), a neurotoxin of herbal and microfungal origin, inhibits succinate dehydrogenase leading thereby to various biochemical and morphological alterations in the brain. Experimental animals treated by 3NP are used to model Huntington's disease. Manganese, often present in occupational settings and as environmental pollutant, inhibits complex II and III of the mitochondria and is known to cause Parkinson-like CNS damage. In this work, rats were administered a single acute dose of Mn (50 mg Mn2+/kg body weight) or 3-NP (20 mg/kg b. w.) and the alterations of the somatosensory cortical evoked potential elicited by stimulation of the whisker pad and the tail base were observed, together with the changes of the action potential in the tail nerve. Latency and amplitude of the two cortical responses changed in parallel, while those of the tail nerve response remained more or less unaltered. The two mitochondrial toxins studied seem to exert their action centrally, primarily on synaptic transmission, rather than peripherally. Recording of evoked activity could be used to follow-up the nervous system effects of mitochondrial toxins, but it requires further investigation.
- Evoked potential
- Mitochondrial toxin
- Nerve action potential
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)
- Agricultural and Biological Sciences(all)