Mitochondrial impairment induced by 3-nitropropionic acid is enhanced by endogenous metalloprotease activity inhibition in cultured rat striatal neurons

Compensatory mechanisms in genetic models of neurodegeneration: are the mice better than humans?

“…Metalloproteases are important in many developmental processes, including cell proliferation, differentiation and migration (Chang and Werb, 2001 ). Endogenous metalloproteases have been proposed to regulate mitochondrial activity in degenerating neurons, and their activation may be regarded as an adaptive and compensatory response to stressful stimuli to protect mitochondrial function (de Oca Balderas et al, 2013 ). Specifically, it has been shown that metalloprotease inhibition stimulates mitochondrial activity impairment induced by 3-nitropropionic acid (3-NP, striatal cell neurotoxin), and metalloproteases may be involved in the cellular reorganization induced by 3-NP (de Oca Balderas et al, 2013 ).…”

Participación de la vía tBHQ-Nrf2 en la protección del daño oxidante por 3NP en ratas viejas

“…El 3NP induce degeneración del caudado-putamen (núcleo estriado) (De Oca Balderas, 2013), causando degeneración en las neuronas espinosas medianas GABAérgicas en el estriado (Beal, 1993), pero también induce lesiones cerebrales en otras áreas localizadas en el hipocampo, tálamo y corteza cerebral (Borlongan, 1997a); estas lesiones están acompañadas de gliosis moderada, disminución en la actividad de la citocromo oxidasa, y una preservación relativa de interneuronas positivas a NADPH diaforasa y aferentes estriatales dopaminérgicas (Bossi, 1993).…”