Impaired nerve conduction velocity in MPTP-treated mouse model of Parkinson's disease

Abstract

Electrophysiological examination can provide valuable information on functional abnormalities in patients with Parkinson's disease (PD). Although there are numerous reports on biochemical and molecular alterations in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced experimental parkinsonism in mice, the mode of electrophysiology in this animal model of PD is not clear. This study provides a comparative evaluation of corticomotor evoked potential (CMEP), compound muscle action potential (CMAP) and motor nerve conduction velocity (NCV) in mice treated with MPTP (30 mg/kg, ip, daily for 4 days) or saline (control group). Although the CMEP latencies were similar in both the groups, the CMEP amplitude was non-significantly decreased in MPTP-treated mice. There was a significant increase in the CMAP latency (1.37 ± 0.03 versus 1.20 ± 0.02 ms) and decrease in CMAP amplitude (4.50 ± 0.89 versus 8.31 ± 0.86 mV) in MPTP-treated mice as compared with control group. This prolonged conduction time resulted in a significant decrease in NCV in MPTP-treated mice (21.98 ± 0.54 m/s) as compared with control mice (24.47 ± 0.33 m/s). There was a significant depletion of striatal dopamine in MPTP-treated animals. These findings demonstrate that systemic administration of MPTP significantly impairs both the central and peripheral nervous systems in mice. However, the resemblance of this neurophysiological status with idiopathic PD or other animal models of PD is not clear and requires additional studies.