An experimental animal model of Huntington’s disease (HD) phenotype was induced with the mycotoxin 3-nitropropionic acid (3-NP) and was well characterized behaviorally, neurochemically, morphometrically, and histologically. Administration of 3-NP caused a decrease in prepulse inhibition (PPI) of the acoustic startle response, locomotor hyperactivity and/or hypoactivity, bilateral striatal lesions, brain oxidative stress, and decreased striatal gamma-aminobutyric acid (GABA) levels.
Taurine is a semi-essential beta-amino acid that has been shown to have both antioxidant and GABA-A agonistic activity. In this study, treatment with taurine (200 mg/kg daily for 3 days) before 3-NP administration reversed both the reduced PPI response and the locomotor underactivity caused by 3-NP injection.
Taurine pretreatment also caused an approximately 2-fold increase in GABA concentration compared with 3-NP-treated animals. In addition, taurine showed antioxidant activity against oxidative stress induced by 3-NP administration, as evidenced by reduced levels of striatal malondialdehyde (MDA) and increased levels of striatal glutathione (GSH). Histochemical examination of striatal tissue showed that prior administration of taurine before 3-NP challenge significantly increased succinate dehydrogenase (SDH) activity compared with 3-NP-treated animals. Histopathological examination further confirmed the neuroprotective effect of taurine in 3-NP-induced HD in rats.
In conclusion, taurine plays a neuroprotective role in the current HD paradigm, which is at least partly due to its indirect antioxidant effect and the agonistic effect of GABA.
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