Shinsuke Nakamura

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PURPOSE To clarify the effects on the visual pathway that occur following retinal damage, we examined the morphological alterations present in the superior colliculus (SC) after N-methyl-D-aspartate (NMDA)-induced retinal damage in mice. METHODS NMDA was injected into the vitreous body of the left eye in mice to induce retinal damage. The time-dependent(More)
Endoplasmic reticulum (ER) stress occurs as a result of accumulation of unfolded or misfolded proteins in the ER and is involved in the mechanisms of various diseases, such as cancer and neurodegeneration. The goal of the present study was to clarify the relationship between ER stress and pathological neovascularization in the retina. Proliferation and(More)
The mouse model of oxygen-induced retinopathy (OIR) has been widely used for studies of retinopathy of prematurity (ROP). This disorder, characterized by abnormal vascularization of the retina, tends to occur in low birth weight neonates after exposure to high supplemental oxygen. Currently, the incidence of ROP is increasing because of increased survival(More)
PURPOSE This study aimed to characterize the functional and morphologic changes in a murine model of ocular ischemic disease caused by vascular occlusion. METHODS Retinal ischemia was induced by unilateral ligation of the pterygopalatine artery (PPA) and the external carotid artery (ECA) in anesthetized mice. Changes in ocular blood flow and retinal(More)
The purpose of this study was to determine whether lomerizine, a Ca(2+) channel blocker, protects against neuronal degeneration within the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) after the induction of retinal damage by intravitreal injection of N-methyl-D-aspartate (NMDA) in mice. NMDA (20 mM/2 microL) was injected into the(More)
The purpose of this study, on mice, was to determine whether memantine, a glutamate-receptor antagonist of the N-methyl-(d)-aspartate (NMDA) subtype, protects against neuronal degeneration in the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) after the induction of retinal damage by intravitreal injection of NMDA. NMDA (20 mM/2(More)
PURPOSE Inflammatory response has a critical role in neuronal damage after retinal ischemia-reperfusion (I/R) injury, and is regulated tightly by the toll-like receptor (TLR) 4. This study aimed to determine whether TLR4 is involved with injury in an ocular ischemic syndrome mice model and to clarify the downstream pathway of TLR4. METHODS To cause(More)
Hypoxic stress is a risk factor of ocular neovascularization. Hypoxia visualization may provide clues regarding the underlying cause of angiogenesis. Recently, we developed a hypoxia-specific probe, protein transduction domain-oxygen-dependent degradation domain-HaloTag-Rhodamine (POH-Rhodamine). In this study, we observed the localization of HIF-1α(More)
Placental growth factor (PlGF) is a member of the vascular endothelial growth factor family. Although it has been reported that PlGF protects against neuronal damage in the brain, little is known about the effects of PlGF in the retina. Therefore, we investigated the effects of PlGF on retinal neuronal cells. To evaluate the effects of PlGF against(More)
Cilostazol is a specific inhibitor of phosphodiesterase III and is widely used to treat ischemic symptoms of peripheral vascular disease. We evaluated the protective effects of cilostazol in a murine model of ocular ischemic syndrome in which retinal ischemia was induced by 5-h unilateral ligation of both the pterygopalatine artery (PPA) and the external(More)