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Neuroprotective effects of topical CB1 agonist WIN 55212-2 on retinal ganglion cells after acute rise in intraocular pressure induced ischemia in rat

Pinar-Sueiro, Sergio; Zorrilla Hurtado, José Ángel; Veiga-Crespo, Patricia LU ; Sharma, Sansar C and Vecino, Elena (2013) In Experimental Eye Research 110. p.8-55
Abstract

Neuroprotection in retinal experimental work consists primarily of preventing retinal ganglion cell (RGC) loss after exposure to a hostile event. We have studied the neuroprotective effect on RGCs in an ischemia-reperfusion model by activation of the cannabinoid receptor CB1 using topical application of WIN 55212-2. Intraocular pressure (IOP) was increased by continuous infusion of phosphate buffer saline (PBS) into the anterior chamber of the eye. Mean intraocular pressure was increased up to 88.5 ± 0.29 mm Hg (control normal IOP 15.1 ± 0.25 mm Hg), for 35 min. Animals were distributed in 3 groups. Left eyes underwent acute rise in intraocular pressure. First group was treated with topical Tocrisolve™ 100 in both eyes. Second group was... (More)

Neuroprotection in retinal experimental work consists primarily of preventing retinal ganglion cell (RGC) loss after exposure to a hostile event. We have studied the neuroprotective effect on RGCs in an ischemia-reperfusion model by activation of the cannabinoid receptor CB1 using topical application of WIN 55212-2. Intraocular pressure (IOP) was increased by continuous infusion of phosphate buffer saline (PBS) into the anterior chamber of the eye. Mean intraocular pressure was increased up to 88.5 ± 0.29 mm Hg (control normal IOP 15.1 ± 0.25 mm Hg), for 35 min. Animals were distributed in 3 groups. Left eyes underwent acute rise in intraocular pressure. First group was treated with topical Tocrisolve™ 100 in both eyes. Second group was treated with 1% solution of CB1 agonist WIN 55212-2 in both eyes. Third group was treated with WIN 55212-2 1% and CB1 antagonist AM 251 1% solutions in both eyes. Subsequently, RGCs were immunolabeled with Brn3a and automated quantification of retinal mosaics of RGCs were performed. The ischemic damage led to a mean loss in RGC density of 12.33%. After topic administration of WIN 55212-2, mean loss of RGCs was of 2.45%. Co-treatment with CB1 antagonist AM 251 abolished almost completely the neuroprotective effect of WIN 55212-2. Topic 1% WIN 55212-2 showed a neuroprotective effect on RGC degeneration after ischemia-reperfusion without pre-activation of CB1 receptors.

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published
keywords
Administration, Topical, Animals, Benzoxazines, Cell Count, Disease Models, Animal, Female, Intraocular Pressure, Morpholines, Naphthalenes, Neuroprotective Agents, Ocular Hypertension, Piperidines, Pyrazoles, Rats, Rats, Sprague-Dawley, Receptor, Cannabinoid, CB1, Reperfusion Injury, Retinal Diseases, Retinal Ganglion Cells, Tonometry, Ocular, Journal Article, Research Support, Non-U.S. Gov't
in
Experimental Eye Research
volume
110
pages
4 pages
publisher
Elsevier
external identifiers
  • scopus:84875653203
ISSN
0014-4835
DOI
10.1016/j.exer.2013.02.009
language
English
LU publication?
no
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6ccbf384-16d8-4b58-87bf-2bbad3f94734
date added to LUP
2016-12-13 14:51:15
date last changed
2018-01-07 11:40:58
@article{6ccbf384-16d8-4b58-87bf-2bbad3f94734,
  abstract     = {<p>Neuroprotection in retinal experimental work consists primarily of preventing retinal ganglion cell (RGC) loss after exposure to a hostile event. We have studied the neuroprotective effect on RGCs in an ischemia-reperfusion model by activation of the cannabinoid receptor CB1 using topical application of WIN 55212-2. Intraocular pressure (IOP) was increased by continuous infusion of phosphate buffer saline (PBS) into the anterior chamber of the eye. Mean intraocular pressure was increased up to 88.5 ± 0.29 mm Hg (control normal IOP 15.1 ± 0.25 mm Hg), for 35 min. Animals were distributed in 3 groups. Left eyes underwent acute rise in intraocular pressure. First group was treated with topical Tocrisolve™ 100 in both eyes. Second group was treated with 1% solution of CB1 agonist WIN 55212-2 in both eyes. Third group was treated with WIN 55212-2 1% and CB1 antagonist AM 251 1% solutions in both eyes. Subsequently, RGCs were immunolabeled with Brn3a and automated quantification of retinal mosaics of RGCs were performed. The ischemic damage led to a mean loss in RGC density of 12.33%. After topic administration of WIN 55212-2, mean loss of RGCs was of 2.45%. Co-treatment with CB1 antagonist AM 251 abolished almost completely the neuroprotective effect of WIN 55212-2. Topic 1% WIN 55212-2 showed a neuroprotective effect on RGC degeneration after ischemia-reperfusion without pre-activation of CB1 receptors.</p>},
  author       = {Pinar-Sueiro, Sergio and Zorrilla Hurtado, José Ángel and Veiga-Crespo, Patricia and Sharma, Sansar C and Vecino, Elena},
  issn         = {0014-4835},
  keyword      = {Administration, Topical,Animals,Benzoxazines,Cell Count,Disease Models, Animal,Female,Intraocular Pressure,Morpholines,Naphthalenes,Neuroprotective Agents,Ocular Hypertension,Piperidines,Pyrazoles,Rats,Rats, Sprague-Dawley,Receptor, Cannabinoid, CB1,Reperfusion Injury,Retinal Diseases,Retinal Ganglion Cells,Tonometry, Ocular,Journal Article,Research Support, Non-U.S. Gov't},
  language     = {eng},
  pages        = {8--55},
  publisher    = {Elsevier},
  series       = {Experimental Eye Research},
  title        = {Neuroprotective effects of topical CB1 agonist WIN 55212-2 on retinal ganglion cells after acute rise in intraocular pressure induced ischemia in rat},
  url          = {http://dx.doi.org/10.1016/j.exer.2013.02.009},
  volume       = {110},
  year         = {2013},
}