Neuroprotection by α2-Adrenergic Receptor Stimulation after Excitotoxic Injury of Chicken Retinal Ganglion Cells: A Population Study
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Retinal ganglion cells (RGCs) loss is one of the most common causes of blindness in worldwide. In this work we studied the RGC population in normal and excitotoxically injured chicken retina after pretreatment with the α2-adrenergic receptor (α2-ADR) agonist brimonidine. The main objective of this work was to study the effects of brimonidine on injured chicken RGCs. A lesion was inflicted by intraocular injection of N-methyl-D-aspartate (NMDA) at embryonic day 18 and the total population of retinal ganglion cells was studied using an automated cell counting of cells positive for the retinal ganglion cell marker Brn3a in flat-mounted retinas. Surviving Brn3a positive RGCs and their distribution in the retina were analyzed 7 and 14 days post lesion. In addition, the total population of retinal ganglion cells was analyzed in a series of normal embryonic day 8 to post-hatch day 11 retinas. The result showed the distribution of total population of RGCs both in embryonic and post-nantal chicken retina. The pretreatment with brimonidine in excitotoxic retina significantly reduced RGC death as seen both 7 and 14 days post lesion. The excitotoxic lesion was more severe in the dorsal quadrants of the retina than in the ventral ones. The regional difference was also seen in the effect of brimonidine. Thus, we conclude that α2-ADR signaling protects RGCs against the excitotoxic injury in the chicken retina.
Alpha2-adrenergic receptor agonist, brimonidine, Brn3a, excitotoxin, flat-mount retina, NMDA, retinal ganglion cells, topographical distribution, development
Research subject Medical Science
IdentifiersURN: urn:nbn:se:uu:diva-281583OAI: oai:DiVA.org:uu-281583DiVA: diva2:914641