Brimonidine tartrate effect on retinal spreading depression depends on Müller cells
Autor: | Adalmir Morterá Dantas, Nassim Calixto, Adroaldo de Alencar, Márcio Penha Morterá Rodrigues, Sebastião Cronemberger, Vinícius Vanzan Pimentel de Oliveira |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
medicine.medical_specialty
genetic structures Retina/efeito de drogas chemistry.chemical_compound Brimonidine Tartrate lcsh:Ophthalmology Ophthalmology medicine Retina Chemistry Nervous tissue Brimonidine Depolarization Retinal Glaucoma Anatomy Inner plexiform layer Agonistas de receptores adrenérgicos alfa 2/uso terapêutico medicine.anatomical_structure lcsh:RE1-994 Cortical spreading depression Retina/drug effects Surgery sense organs Adrenergic alpha-2 receptor agonists/therapeutic use medicine.drug |
Zdroj: | Revista Brasileira de Oftalmologia v.73 n.6 2014 Revista Brasileira de Oftalmologia Sociedade Brasileira de Oftalmologia (SBO) instacron:SBO Revista Brasileira de Oftalmologia, Vol 73, Iss 6, Pp 335-340 (2014) |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |