Author(s): Vasiljević Ivana, Jovanović Marina, Čolić M, Mišić D, Ninković Milica, Maličević Ž
Keywords:acetylcholinesterase, Huntington disease, nerve growth factor, quinolinic acid.
The etiology of neuronal death in neurodegenerative diseases, including Huntington's disease (HD) is still unknown. There could be a complex interplay between altered energy metabolism, excitotoxicity and oxidative stress. Excitotoxic striatal lesions induced by quinolinic acid (QA), were used to test for the neuroprotective actions of nerve growth factor (NGF) on striatal cholinergic and GABAergic neurons. QA is an endogenous excitotoxin acting on N-methyl-D-aspartate (NMDA) receptors, that leads to neurotoxic damage resembling the alterations observed in HD. Unilateral administration of QA, in to the rat striatum in a single dose of 150 nM/L was used as the model of Huntington's disease. The second group was treated both with QA in the same dose and NGF in a dose of 7x10-9 g. NGF was applied immediately before the neurotoxin. The control group was treated with 0.154 mmol/L saline solution likewise. The activity of acetylcholinesterase (AChE) was increased in both the ipsi- and contralateral striatum, forebrain cortex, hippocampus and basal forebrain of QA-treated animals. This was prevented by NGF Some evidence suggests that interaction between neurotrophin receptors and glutamatergic activity may play an important role in plastic changes and synaptic reorganization of striatal circuits after excitotoxic injury. Considering that NGF mediates their activity across glutamatergic synapses, and, besides others, also has antioxidative effects, the obtained results indicate its protective role towards functional defects caused by QA.
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