This week BMC Seminar will be this Thursday 21st November 12:00-12:40 by Guðmundur Jónsson
Title: Stimulation and inhibition of retinal A2A and A3 adenosine receptors and their effect on the components of the rat ERG
Title in Icelandic: Örvun og hömlun sjónhimnu A2a og A3 adenosine viðtaka og áhrif þeirra á rottu ERG
Abstract: The electroretinogram (ERG) is an electrical signal generated by the retina that can be recorded by placing electrodes on the cornea and the eyelids. It consists of several separate components that appear in the response at distinct time points after stimulation by a flash of light. The most prominent among them are the a-wave, b-wave and the oscillatory potentials. Adenosine is a neuromodulator that can be found in various areas of the central nervous system, including the retina. The purpose of this study was to examine what role adenosine receptors may play in the generation of the ERG.
Sprague Dawley rats were anesthetized by an intraperitoneal injection of S-ketamine (75mg/kg) and xylazine (6mg/kg). ERG was recorded with a corneal ERG electrode. Adenosine agonist CGS21680 and antagonist ZM241385 for A2A receptors, and adenosine agonist 2-CI-IB-MECA and antagonist VUF5574 for A3 receptors along with exogenous adenosine were injected into the vitreous and their effects on the ERG components were examined, along with ERG flicker responses.
Both A3 agonist 2-CI-IB-MECA and antagonist VUF5574 along with exogenously applied adenosine caused a significant statistical increase in the amplitude of the a–wave, while the A2A agonist CGS21680 and antagonist ZM241385 did not. The b-wave of the ERG of the dark adapted retina decreased in amplitude in all cases except for VUF5574 and exogenously applied adenosine, which both increased the amplitude. The changes in the amplitude of the b-wave were statistically significant for all ligands except ZM241285. The changes in the ERG of the light adapted retina induced by A3 and A2A agonists were statistically significant, while the A2A and A3 antagonists did not have a significant effect. Both agonists decreased the amplitude of the ERG of the light adapted retina. The amplitude of the scotopic oscillatory potentials was significantly decreased by injection of either an A2A or A3 agonist. None of the ligands tested caused a significant change in the amplitude of the flicker response.
The results show that the ERG is influenced by both adenosine receptors to varying degrees. All the ligands tested along with exogenous adenosine had a significant statistical effect on one ERG component or another. The only exception to this was the A2A antagonist who had no significant statistical effect on any of the ERG components. Stimulation of both A3 and A2A causes reduction in the scotopic ERG b-wave. Stimulation of A2A and A3 receptors also causes a reduction in the photopic ERG b-wave. Blocking the A3 adenosine receptor with an antagonist caused an increase in the scotopic ERG a- and b-wave. Only the receptor agonists affect the oscillatory potentials. Interestingly exogenous adenosine doesn’t have any effect on either the oscillatory potentials or the photopic b-wave. Retinal neurons that contain A2A and/or A3 adenosine receptors contribute to the generation of the ERG b-wave and oscillatory potentials.
Image is from following webpage: http://webvision.med.utah.edu/book/part-i-foundations/simple-anatomy-of-the-retina/