Summary.
The aim of this study was to evaluate the effect of MPTP (2 × 45 mg/kg s.c., 20 h apart) on striatal neuropeptide Y-like immunoreactivity (NPY-LI) in C57BL/6 mice. NPY-LI markedly increased 2 weeks after MPTP but it remained unchanged after 24 h, 1 or 6 weeks. The increase in NPY-LI was accompanied by depletion of dopamine (−80%), DOPAC (−70%), 3-MT (−44%) and HVA (−52%). L-Deprenyl completely prevented the MPTP-induced NPY-LI increase, neurodegeneration of the striatal dopamine system and motor dysfunction. Clonidine attenuated the neurotoxin effect on NPY-LI and dopaminergic neurons. L-dopa/carbidopa protected NPY neurons against MPTP but slightly enhanced MPTP-induced decrease in the levels of dopamine and its metabolites. The relationship between changes in NPY-LI and dopamine and serotonin metabolism determined by HPLC was discussed. The results further extend the range of MPTP-elicited modifications in striatum and demonstrate that drugs with antiparkinsonian activity can protect NPY neurons against MPTP toxicity.
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Obuchowicz, E., Antkiewicz-Michaluk, L., Romańska, I. et al. Increased striatal neuropeptide Y immunoreactivity and its modulation by deprenyl, clonidine and L-dopa in MPTP-treated mice. J Neural Transm 110, 1375–1391 (2003). https://doi.org/10.1007/s00702-003-0047-1
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DOI: https://doi.org/10.1007/s00702-003-0047-1