Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype

Treatment with taurine (200 mg/kg daily for 3 days) prior to 3-NP administration reversed reduced prepulse inhibition and locomotor hypoactivity.

• Administration of the mycotoxin 3-NP resulted in reduced prepulse inhibition and locomotor activity in an animal model of Huntington's disease.
• 3-NP treatment was associated with bilateral striatal lesions, brain oxidative stress, and decreased levels of gamma-aminobutyric acid (GABA).
• Taurine pretreatment caused approximately a 2-fold increase in GABA concentration compared to animals treated with 3-NP alone.
• Taurine also demonstrated antioxidant activity, evidenced by reduced levels of malondialdehyde and elevated glutathione in the striatum after 3-NP administration.
• Histochemical examination revealed significantly increased succinate dehydrogenase activity in striatal tissue following taurine administration prior to 3-NP exposure.
• Overall, taurine appears to have a neuroprotective role in this Huntington's disease model due to its antioxidant effects and GABA agonistic properties.

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