Neuroprotective effects of topical CB1 agonist WIN 55212-2 on retinal ganglion cells after acute rise in intraocular pressure induced ischemia in rat
(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.
(Less)
- author
- Pinar-Sueiro, Sergio ; Zorrilla Hurtado, José Ángel ; Veiga-Crespo, Patricia LU ; Sharma, Sansar C and Vecino, Elena
- publishing date
- 2013-05
- type
- Contribution to journal
- publication status
- 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
-
- pmid:23454099
- scopus:84875653203
- ISSN
- 0014-4835
- DOI
- 10.1016/j.exer.2013.02.009
- language
- English
- LU publication?
- no
- id
- 6ccbf384-16d8-4b58-87bf-2bbad3f94734
- date added to LUP
- 2016-12-13 14:51:15
- date last changed
- 2024-07-28 00:58:34
@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}}, 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}}, 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}}, doi = {{10.1016/j.exer.2013.02.009}}, volume = {{110}}, year = {{2013}}, }