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Original

Exp Neurobiol 2003; 12(2): 127-133

Published online December 31, 2003

© The Korean Society for Brain and Neural Sciences

Changes of Calbindin-D28k-containig Neurons on the Substantia Nigra of 6-Hydroxy Dopamine Induced Parkinsonian Rat Models

Young-Bok Yoo*

Department of Anatomy, College of Medicine, Dankook University, Cheonan, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 041-550-3856, FAX: 041-550-3905
e-mail: ybyoo36@hanmail.net
The present research was conducted by the research fund of Dankook University in 2003.

Abstract

Parkinson's disease is the motor disorder which results from the selective degeneration of the dopaminergic neurons in the substantia nigra (SN) and the deficiency of dopamine in the corpus striatum (CS). But etiological factors are still unknown. In this study, we made parkinsonian rat models which were under oxidative stress injecting 6-OHDA in SN. According to the time transition after neurotoxin injection we made the coronal sections of SN immunohistochemical staining by anti-Tyrosine hydroxylase (TH) and calbindin-D28K antibody. We compared the survival rate (%) of calbindin-D28K- immunoreactive cells with that of TH-immunoreactive cells to confirm the suggested role of calbindin-D28K which may protect dopaminrgic neurons against the cytotoxicity according to the time transition after 6-OHDA injection. In parkinsonian rat models which were sacrificed 7 d, 10 d, 14 d, 17 d after the injection of 6-OHDA, the survival rates of calbindin-D28K-immunoreactive neurons is significantly higher than that of TH- immunoreactive neurons (p>0.05). We suggest that calbindin-D28K containing neurons tend to be spared during the acute period of parkinsonian rat models, calbindin-D28K helps to protect neurons against excitotoxicity. This is consistent with the proposed calbindin-D28K function as an intraneuronal calcium buffer.

Keywords: Calbindin-D28K, TH, Parkinson's disease, substantia nigra, rat