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Editors Selection IGR 21-2

Basic science: Excitotoxicity - glutamate

Comment by Manuel Vidal-Sanz on:

12578 Neurochemical evidence to implicate elevated glutamate in the mechanisms of high intraocular pressure (IOP)-induced retinal ganglion cell death in rat, Nucci C; Tartaglione R; Rombola L et al., Neurotoxicology, 2005; 26: 935-941

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In a model of retinal ischemia induced by transient elevation of the intraocular pressure, Nucci et al. (840) examine the implication of excitotoxicity in the loss of retinal neurons in the ganglion cell layer.

In adult rats, transient ischemia of the retina was induced by elevation of the intraocular pressure for 45 minutes. This type of insult leads to loss of retinal neurons which was observed as early as six hours after the insult. The loss of retinal neurons coincided with the appearance of morphological characteristics of apoptosis (chromatin marginalization and condensation as well as TUNEL-positive cells). The loss of retinal neurons, as shown previously, proceeds with longer reperfusion intervals.

The role of glutamate mediated excitotoxicity in this loss of retinal neurons is suggested by two concomitant observations in these experiments. 1) An increased level of glutamate in the living rat retina, as detected with micro dialysis and high-performance liquid chromatography (HPLC). Interestingly, elevated levels of glutamate appeared in the early reperfusion period, two hours after ischemia and only in five out of eight animals tested. 2) The effects of systemic treatment with selective antagonists of the N-methyl-D-aspartate (NMDA) and non-NMDA subtypes of glutamate receptors, in preventing or diminishing RGC loss. Moreover, pre-treatment with MK 801 (a NMDA receptor antagonist) resulted in prevention of glutamate increase seen two hours after ischemia.

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