An improved model for examining delayed excitotoxic neurodegeneration in isolated chick retina.
Extensive use of the embryonic chick retina model has been made for examining mechanisms of acute excitotoxicity. The standard retina model does not, however, address the concept of delayed excitotoxicity. In previous retina based studies extending the time course to 24 h has proven problematic owing to damage arising in control tissue. Recently a model for examining delayed excitotoxicity in isolated retina was proposed. This method relied on a significant reduction in incubating temperature to avoid the variable damage occurring in control tissue. The data in the present study suggest that a reduction in temperature results in N-methyl-D-aspartate (NMDA) receptor dysfunction, preventing accurate assessment of NMDA receptor mediated excitotoxicity. An improved model is proposed which permits incubation at 37 degrees C without damage occurring in control tissue.
Eggett
C J
CJ
Department of Biomedical Science, University of Sheffeld, UK.
O'Leary
T A
TA
Reynolds
G P
GP
D000818:Animals; D002642:Chick Embryo; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D008959:Models, Neurological; D009410:Nerve Degeneration / Q000502:physiology*; D012160:Retina / Q000187:drug effects*
D018698:Glutamic Acid; D007770:L-Lactate Dehydrogenase; D005947:Glucose