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Abstract #21962 Published in IGR 10-4

17β-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat

Russo R; Cavaliere F; Watanabe C; Nucci C; Bagetta G; Corasaniti MT; Sakurada S; Morrone LA
Progress in Brain Research 2008; 173: 583-590

See also comment(s) by Abbot Clark


Glaucoma, is a progressive optic neuropathy often associated with increased intraocular pressure (IOP) and characterized by progressive death of retinal ganglion cells (RGCs). High acute rise of IOP is a model for retinal ischemia and may represent a model of acute angle closure glaucoma. Here we have used this experimental model in combination with a neurochemical and neuropathological approach to gain more insight in the neuroprotective profile of 17β-estradiol (E2), a steroid hormone, which has been shown to increase the viability, survival, and differentiation of primary neuronal cultures from different brain areas including amygdala, hypothalamus, and neocortex. Our data demonstrate that systemic administration of E2 significantly reduces RGC loss induced by high IOP in rat. In addition, pretreatment with E2, 30 min before ischemia, minimizes the elevation of glutamate observed during the reperfusion period. These effects seem to be in part mediated by the activation of the estrogen receptor, since a pretreatment with ICI 182-780, a specific estrogen receptor antagonist, partially counteracts the neuroprotection afforded by the estrogen.

Dr. L.A. Morrone, Department of Pharmacobiology, University of Calabria, 87036 Arcavacata di Rende, Italy. luigimorron@libero.it


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