Systemic 3-nitropropionic acid: Behavioral deficits and striatal damage in adult rats

3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum

“…For example, 3-nitropropionic acid (3-NP) induces striatal neuronal damage in humans and experimental animals [11,12] . This mitochondrial toxin inhibits mitochondrial complex II in the respiratory chain, reduces ATP synthesis, increases Ca 2+ influx, and activates proteases that cause cellular damage and the death of medium spiny neurons [12][13][14] .…”

Ischemic tolerance in chemical preconditioning: Possible role of astrocytic glutamine synthetase buffering glutamate‐mediated neurotoxicity

“…3-NPA is a suicide inactivator of SDH in the TCA cycle (Coles et al, 1979;Calabresi et al, 2001), and the striatum is the most vulnerable region in the brain to systemic intoxication with high dose injection of 3-NPA (Borlongan et al, 1995;Alexi et al, 1998;Nakahara et al, 2001;Brownell et al, 2004). Several studies have shown, however, that a single administration of 3-NPA given systemically provides cerebral ischemic tolerance in focal ischemic models (Wiegand et al, 1999;Horiguchi et al, 2003;Pera et al, 2004;Zhu et al, 2004;Hoshi et al, 2005).…”

Comparative Study on 3-Nitropropionic Acid Neurotoxicity

“…The main advantage of 3-NPA over the excitotoxins is that selective striatal lesions can be accomplished via systemic administration, and therefore the animal is not exposed to surgical trauma associated with intraparenchymal injections of the neurotoxin ( Table 1). The systemic 3-NPA model is regarded also as a more improved model than intrastriatal 3-NPA model because, in addition to the former's technical advantages as mentioned previously, systemic 3-NPA administration has higher selectiv- ity in producing striatal lesions compared to intrastriatal 3-NPA injection which produces widespread extrastriatal damage (1)(2)(3)(4). In the argument that we recently presented (5), systemic administration of 3-NPA in rodents can parallel the evolution of HD whereas the intraparenchymal injections of excitotoxins (and also noted in intrastriatal3-NPA infusion) (3,4) can only mimic specific stages of the disease.…”