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Vol. 296, Issue 1, 216-223, January 2001
2-Adrenoceptor Agonists Inhibit Vitreal Glutamate
and Aspartate Accumulation and Preserve Retinal Function after
Transient Ischemia
Department of Biological Sciences, Allergan, Inc., Irvine,
California
Recent studies have suggested that 
2-adrenergic agonists
prevent neuronal cell death in a number of animal models, although the
mechanism of 2-neuroprotection remains unclear. In a
retinal ischemia model, the 2-specific agonist
brimonidine (1 mg/kg i.p.) preserves approximately 80% of the
electroretinogram (ERG) b-wave. The protective effect of brimonidine is
completely blocked by coadministration of the 2-
antagonist rauwolscine. Brimonidine treatment preserves the ERG b-wave
if animals are treated 1 or 3 h before ischemia, but has no effect
if it is injected during ischemia. The 3-h pretreatment effect is
blocked by i.v. injection of rauwolscine 2 h later (1 h before
ischemia). A comparison of vitreous humor glutamate levels between
untreated and brimonidine-treated eyes shows that 1) after ischemia,
glutamate levels rise 2- to 3-fold in the untreated animals, and 2)
glutamate levels in the brimonidine-treated animals are comparable to
the nonischemic controls. Hence, the mechanism for brimonidine-mediated
protection in the retinal ischemia model requires activation of the
2-adrenergic receptors immediately before and during
ischemia. These data suggest that activation of the
2-adrenergic receptor may reduce ischemic retinal injury
by preventing the accumulation of extracellular glutamate and aspartate.
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