Lee Jiyong, Park Kichul, Lee Sungsoo, Whang Kum, Kang Minjeong, Park Chan, Huh Youngbuhm
Department of Neurology, Wonju College of Medicine, Yonsei University, Ilsan-Dong 162, Wonju, Gangwon-Do, 220-701South Korea.
Neurosci Lett. 2002 Nov 22;333(2):87-90. doi: 10.1016/s0304-3940(02)00987-4.
It has been suggested that calcium binding proteins protect against Ca2+ overload, thus rendering neurons more resistant against excitotoxicity. The influence of kainic acid, which induces status epilepticus, on the expressions of calbindin D28k, parvalbumin and calretinin was examined in the rat striatum by immunohistochemistry and microdensitometry. At 1, 3 and 6 days after kainic acid-induced seizure, the number of calretinin-positive neurons in the striatum was significantly lower than in control rats. However, no significant difference was observed in the number of calbindin D28k- and parvalbumin-positive neurons in control and seizure rats. At 1, 3 and 6 days after seizure the optical densities of calretinin- and parvalbumin-positive neurons in the striatum were significantly lower than in control rats. Our finding concerning the selective loss of calretinin-positive neurons in seizure groups suggests that calcium binding proteins in the striatum have differential vulnerabilities to kainic acid-induced seizure.
