Isatin, an endogenous MAO inhibitor, improves bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by Japanese encephalitis virus

Ogata, Akihiko; Hamaue, Naoya; Terado, Mutsuko; Minami, Masaru; Nagashima, Kazuo; Tashiro, Kunio

« Previous Next »Journal of the Neurological Sciences
Volume 206, Issue 1 , Pages 79-83, 15 January 2003

Isatin, an endogenous MAO inhibitor, improves bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by Japanese encephalitis virus

Akihiko Ogata
- Corresponding author. Tel.: +81-11-716-1161x6028; fax: +81-11-700-5356.
- Department of Neurology, Hokkaido University School of Medicine, Kita-14, Nishi-5, Kita-ku, Sapporo 060-8648, Japan
Naoya Hamaue
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Science University of Hokkaido, Ishikari-Tobetsu, Japan
Mutsuko Terado
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Science University of Hokkaido, Ishikari-Tobetsu, Japan
Masaru Minami
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Science University of Hokkaido, Ishikari-Tobetsu, Japan
Kazuo Nagashima
- Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan
Kunio Tashiro
- Department of Neurology, Hokkaido University School of Medicine, Kita-14, Nishi-5, Kita-ku, Sapporo 060-8648, Japan

Received 29 January 2002; received in revised form 17 July 2002; accepted 28 August 2002.

Abstract

Isatin, an endogenous monoamine oxidase (MAO) inhibitor, has an important role in the control of neurotransmitter concentration. We previously reported that exogenously administered isatin significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. In order to test the possibility of treating Parkinson's disease by isatin, we evaluated DA levels in the striatum and bradykinesia using a rat model of Parkinson's disease induced by the Japanese encephalitis virus (JEV).

We have already reported that in adult Fischer rats infected with JEV at day 13, there was a marked decrease of tyrosine hydroxylase-positive neurons in the bilateral substantia nigra after 12 weeks. Effects of isatin were investigated in JEV-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatograph (HPLC) with an electrochemical detector (ECD). Isatin (100 mg/kg per day for 1 week, intraperitoneal injection) improved the bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. Isatin also increased DA in the striatum of parkinsonism rats. These results suggest that isatin could be a possible treatment for Parkinson's disease as well as for post-encephalitic parkinsonism.

Keywords: Japanese encephalitis virus, Post-encephalitic parkinsonism, Parkinson's disease, Isatin, Monoamine oxidase inhibitor, Treatment