Excitotoxic Cell Death in Cultured Retinal Neurons.
- Author:
Young Hee YOON
1
;
Myoung Ja SHIM
;
Jaeheung LEE
Author Information
1. Department of Ophthalmology, Ulsan University, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
AMPA/kainate receptor;
Cultured retinal neurnos;
Excitotoxicity;
GABAergic neuron;
Glu R2 subunit
- MeSH:
6-Cyano-7-nitroquinoxaline-2,3-dione;
Animals;
Calbindins;
Cell Death*;
Cobalt;
Dizocilpine Maleate;
GABAergic Neurons;
Ganglion Cysts;
Humans;
Infant, Newborn;
Kainic Acid;
N-Methylaspartate;
Neurons;
Rats;
Receptors, Kainic Acid;
Retinal Neurons*;
Retinaldehyde*
- From:Journal of the Korean Ophthalmological Society
1997;38(11):1987-1999
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
We examined excitotoxicity, putatively a major mechanism of ischemic neuronal death, in primary rat retinal cultures. Retinal cultures were prepared from newborn rats (day 1 or 2). Exposure of these cultures (DIV8-10)to NMDA or kainate induced neuronal death. Furthermore, MK-801 or CNQX each partially attenuated glutamateinduced neuronal death, suggesting that both NMDA and kainate receptors mediate it. Thy-1(+) retinal ganglion neurons, like neurons as a whole, were equally injured by NMDA and by kainate. However, GABA(+) or calbindin (+) neurons of the inner nuclear layer were resistant to NMDA, but highly vulnerable to kainate. These neurons may have AMPA/kainate receptors that are highly permeable to Ca2+, as they take up cobalt with kainate stimulation. These results suggest that the AMPA/kainate receptor, rater than the NMDA receptor, may mediate this pattern of selective neurnonal death.
