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Titill: 
  • Titill er á ensku The effects of stimulating or blocking the retinal A2A and A3 adenosine receptors on the components of the rat electroretinogram
  • Áhrif örvunar eða hömlunar sjónhimnu A2A og A3 adenosine viðtaka á þætti sjónhimnurits rottu
Leiðbeinandi: 
Skilað: 
  • Október 2014
Útdráttur: 
  • Útdráttur er á ensku

    Adenosine is a neuromodulator that is present in various areas of the central nervous system, including the retina. It has been suggested that adenosine may serve a neuroprotective role in the retina, based on electroretinogram (ERG) recordings from the rat retina. The purpose of this study was to assess the role of A2A and A3 adenosine receptors, known to be present in the rat retina, in generation and modulation of the rat ERG.
    Sprague Dawley rats were anesthetized by an intraperitoneal injection of S-ketamine (75mg/kg) and xylazine (6mg/kg). The flash ERG was recorded between an electrode placed on the cornea and a reference electrode on the lower canthus. An agonist and antagonist for A2A receptors, and an agonist and antagonist for A3 receptors, in addition to exogenous adenosine were each injected (5 µL) into the vitreous of six eyes with a NanoFil IOKit system (World Precision Instruments, Inc, USA). Their effects on the components of the scotopic and photopic ERGs were examined, along with ERG flicker responses.
    Exogenous adenosine [0.5 mM] caused an increase in the mean amplitude of the scotopic ERG a-wave from 68.0 ± 7.7 µV to 96.7 ± 13.7 µV (p=0.042). It also increased the mean amplitude of the scotopic b-wave from 236.5 ± 38.4 µV to 305.3 ± 41.6 µV (p=0.035). The A2A agonist CGS21680 [2mM] decreased the mean amplitude of both the ERG b-wave of dark adapted (298.2 ± 21.5 µV to 212.5 ± 19.3 µV; p=0.005) and light adapted eyes (124.3 ± 17.7 µV to 87.8 ± 11.2 µV; p=0.045). The mean scotopic oscillatory potentials were also decreased by the injection of CGS21680 (99.9 ± 9.4 µV to 47.2 ± 11.4 µV; p=0.023). ZM241385 [4mM] which is an A2A antagonist did not have any effect on any component of the ERG. The A3 agonist 2-CI-IB-MECA [0.5mM] increased the mean amplitude of the a-wave (91.4 ± 15.4 µV to 152.9 ± 21.2 µV; p=0.006), while causing a decrease in the mean amplitude of the b-waves of both dark adapted (290.9 ± 40.3 µV to 210 ± 21.4 µV; p=0.022) and light adapted (170 ± 19 µV to 135.9 ± 11.4 µV; p=0.037) eyes. The scotopic oscillatory potentials likewise decreased in mean amplitude (79.6 ± 15.2 µV to 39.2 ± 3.9 µV; p=0.038) by 2-Cl-IB-MECA. The A3 antagonist VUF5574 increased the mean amplitude of both the a-wave (65.8 ± 8.0 µV to 139.5 ± 29.3 µV; p=0.046) and the b-wave of dark adapted eyes (223.7 ± 20.3 µV to 312 µV ± 38.7 µV; p=0.037). None of the ligands tested had any effect on the ERG flicker response.
    Retinal neurons that contain A2A and/or A3 adenosine receptors contribute to the generation of the ERG a- and b-waves and oscillatory potentials.

Samþykkt: 
  • 30.9.2014
URI: 
  • http://hdl.handle.net/1946/19854


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