Current eye research · 1996
Disturbances in the distribution of neurotransmitters in the rat retina after ischemia.
СтатьяПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Perlman J I, McCole S M, Pulluru P, Chang C J, Lam T T, Tso M O
Аннотация
PURPOSE: Disturbances in neurotransmitter distribution have been observed in cerebral ischemia in the pathophysiologic process of excitotoxicity. The goal of this study was to examine the effect of pressure-induced retinal ischemia on the distribution of the retinal neurotransmitters glutamate and gamma-aminobutyric acid (GABA) within the rat retina.
METHODS: Animals were subjected to increased intraocular pressure of 110 mm Hg for 45 min using an intracameral hydrostatic pressure device. The distribution of glutamate and GABA immunoreactivity (IR) was determined at 0, 2, 4, 8 and 24 hrs after reperfusion by immunogold with silver intensification.
RESULTS: Three phases of neurotransmitter immunoreactivity patterns were discernible following retinal ischemia. Immediately following reperfusion (Phase I), a shift of GABA-IR from inner retinal neurons to the Mueller cells and their processes was noted. In contrast, despite marked decreases in neuronal glutamate-IR, a less pronounced shift of glutamate-IR to the Muller cells was simultaneously noted. This shift of neurotransmitter IR to the Mueller cells was transient with the gradual reappearance of IR within the inner retinal neurons noted 2-8 hrs after reperfusion (Phase II). Phase III began at 8 hrs after reperfusion with progressive loss of GABA-IR noted in the inner retina; by 24 hrs, secondary loss of inner retinal glutamate-IR was evident with corresponding dropout and pyknosis of inner retinal neurons apparent.
CONCLUSIONS: The distribution of glutamate-IR and GABA-IR was significantly altered following retinal ischemia. The alteration noted in Phase I suggested that the regulation of glutamate by Mueller cells was disrupted by this ischemic insult leading to glutamate excitotoxicity, and delayed neuronal cell degeneration as evidenced by the subsequent loss of inner retinal immunoreactivity in Phase III.
METHODS: Animals were subjected to increased intraocular pressure of 110 mm Hg for 45 min using an intracameral hydrostatic pressure device. The distribution of glutamate and GABA immunoreactivity (IR) was determined at 0, 2, 4, 8 and 24 hrs after reperfusion by immunogold with silver intensification.
RESULTS: Three phases of neurotransmitter immunoreactivity patterns were discernible following retinal ischemia. Immediately following reperfusion (Phase I), a shift of GABA-IR from inner retinal neurons to the Mueller cells and their processes was noted. In contrast, despite marked decreases in neuronal glutamate-IR, a less pronounced shift of glutamate-IR to the Muller cells was simultaneously noted. This shift of neurotransmitter IR to the Mueller cells was transient with the gradual reappearance of IR within the inner retinal neurons noted 2-8 hrs after reperfusion (Phase II). Phase III began at 8 hrs after reperfusion with progressive loss of GABA-IR noted in the inner retina; by 24 hrs, secondary loss of inner retinal glutamate-IR was evident with corresponding dropout and pyknosis of inner retinal neurons apparent.
CONCLUSIONS: The distribution of glutamate-IR and GABA-IR was significantly altered following retinal ischemia. The alteration noted in Phase I suggested that the regulation of glutamate by Mueller cells was disrupted by this ischemic insult leading to glutamate excitotoxicity, and delayed neuronal cell degeneration as evidenced by the subsequent loss of inner retinal immunoreactivity in Phase III.