Abstract
Objective: Demonstrate the Brimonidine effect over Retinal Spreading Depression (SD). Brimonidine is an alpha-2–adrenergic receptor agonist, used in the management of glaucoma. Alpha2-agonists have been shown to be neuroprotective in various experimental models, however the molecular and cellular targets leading to these actions are still poorly defined. The SD of neuronal electric activity is a wave of cellular massive sustained depolarization that damages the nervous tissue. Local trauma, pressure, ischemic injuries and other chemical agents as high extracellular potassium concentration or glutamate, can trigger SD, leading to exaggerated focal electrical followed by an electrical silence. Methods: Using chicken retina as model, we performed alpha2-receptor detection by Western Blotting and Immunohistochemistry. After that we obtained electrical signals of SD by microelectrodes on retina in the absence or presence of Brimonidine. For in vivo visualization we observed retina with optical coherence tomography on normal state, with SD passing, and with SD + Brimonidine. Results: Our data demonstrated that: (1) alpha2-adrenergic receptors are present in Muller cells, (2) the treatment with Brimonidine decreases the SD‘s velocity as well as the voltage of SD waves and (3) OCT revealed that SD creates a hyper reflectance at inner plexiform layer, but on retinal treatment with brimonidine, SD was not visualized. Conclusions: Our study about brimonidine possible pathways of neuroprotection we observed it reduces SD (a neuronal damage wave), identified a new cellular target – the Muller cells, as well as, firstly demonstrated SD on OCT, showing that the inner plexiform layer is the main optically affected layer on SD.
Highlights
Glaucoma is an optic nerve disease generally characterized by elevated intraocular pressure (IOP)
All the three alpha-2adrenergic receptor are widely distributed in the nervous system, the a2A and a2C subtypes appear to predominate in central nervous system (CNS)[16]
Several clinical studies document its safety and efficacy[20,21,22] more recent experimental and animal models suggest a neuroprotective effect of Brimonidine
Summary
Glaucoma is an optic nerve disease generally characterized by elevated intraocular pressure (IOP). Besides the elevated IOP, glaucoma is best defined as a neurodegenerative disease characterized by the slow, progressive degeneration of retinal ganglion cells (RGCs), which is manifested initially as visual field loss and, irreversible blindness if left untreated. Glaucoma is the second leading cause of blindness in the world, and the first cause of irreversible blindness. It is estimated that there are 60 million people worldwide affected by glaucoma and 8.4 million being bilaterally blind. The precise cause of RGCs death in glaucoma is unknown, several mechanisms have been proposed. These include: mechanical compression due to elevated IOP, neurotrophic factor deprivation, excitotoxicity, ischemia, hypoxia and oxidative stress. Because conventional treatment to reduce IOP does not always prevent progression of glaucomatous neurodegeneration, recent research in glaucoma has been focused on the alternative treatment strategies as the neuroprotection[2]
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