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Journal of the Korean Ophthalmological Society ; : 1987-1999, 1997.
Article in Korean | WPRIM | ID: wpr-55063

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.


Subject(s)
Animals , Humans , Infant, Newborn , Rats , 6-Cyano-7-nitroquinoxaline-2,3-dione , Calbindins , Cell Death , Cobalt , Dizocilpine Maleate , GABAergic Neurons , Ganglion Cysts , Kainic Acid , N-Methylaspartate , Neurons , Receptors, Kainic Acid , Retinal Neurons , Retinaldehyde
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