J Korean Ophthalmol Soc.  1997 Nov;38(11):1987-1999.

Excitotoxic Cell Death in Cultured Retinal Neurons

• Yoon YH
• Shim MJ
• Lee J

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.

Keyword

AMPA/kainate receptor; Cultured retinal neurnos; Excitotoxicity; GABAergic neuron; Glu R2 subunit

MeSH Terms

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*
6-Cyano-7-nitroquinoxaline-2,3-dione
Cobalt
Dizocilpine Maleate
Kainic Acid
N-Methylaspartate
Receptors, Kainic Acid
Retinaldehyde