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Updated: Aug 29, 2026
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Published on: January 7, 2014
Increased striatal neuropeptide Y immunoreactivity and its modulation by deprenyl, clonidine and L-dopa in
E Obuchowicz1, L Antkiewicz-Michaluk, I Romańska
1Department of Clinical Pharmacology, Silesian Medical University, Katowice, Poland. eobuchowicz@slam.katowice.pl
Abstract:
The aim of this study was to evaluate the effect of MPTP (2 x 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.
Insights
MPTP neurotoxin increases neuropeptide Y-like immunoreactivity (NPY-LI) in mice striatum. Antiparkinsonian drugs like L-Deprenyl protect against MPTP toxicity and motor deficits.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a neurotoxin used to model Parkinson's disease.
- Neuropeptide Y (NPY) is implicated in various neurological functions, including stress and neuroprotection.
Purpose of the Study:
- To investigate the impact of MPTP administration on NPY-like immunoreactivity (NPY-LI) in the mouse striatum.
- To assess the neuroprotective effects of L-Deprenyl, Clonidine, and L-dopa/carbidopa against MPTP-induced changes.
Main Methods:
- C57BL/6 mice were administered MPTP (2 x 45 mg/kg s.c., 20 h apart).
- NPY-LI, dopamine, DOPAC, 3-MT, and HVA levels were measured at various time points using HPLC.
- Effects of L-Deprenyl, Clonidine, and L-dopa/carbidopa were evaluated.
Main Results:
- MPTP significantly increased striatal NPY-LI 2 weeks post-administration, accompanied by dopamine depletion.
- L-Deprenyl completely prevented MPTP-induced NPY-LI increase, dopaminergic neurodegeneration, and motor dysfunction.
- Clonidine and L-dopa/carbidopa showed partial protection of NPY neurons and dopaminergic system.
Conclusions:
- MPTP induces significant alterations in striatal NPY-LI and dopaminergic metabolism.
- Antiparkinsonian drugs demonstrate neuroprotective potential against MPTP toxicity.
- NPY neurons are vulnerable to MPTP, and their protection may be a therapeutic target.
