Effect of Memantine on Neuroretinal Function and Retinal Vascular Changes of Streptozotocin-Induced Diabetic Rats

Kusari, Jyotirmoy; Zhou, S.; Padillo, E.; Clarke, Kevin; Gil, Daniel W.

doi:10.1167/iovs.07-0427

Cited by 114 publications

(93 citation statements)

References 52 publications

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“…The number of retinal ganglion cells were counted on each photograph automatically using a software system (CPAS software, Daheng software Ltd, Beijing, China). 7 About 500-700 cells per eye were counted. The photographs covered a retinal area of about 0.25 mm 2 .…”

Section: Methodsmentioning

confidence: 99%

“…It has, therefore, been desirable to develop treatment strategies by which the retina and optic nerve can be protected from degeneration by helping the retinal cells to survive even under difficult conditions. Recent studies have reported that substances such as ciliary neurotrophic factor, [3][4][5] brain-derived growth factor, 6 memantine, 7,8 and Ginkgo biloba may have a stabilizing or protecting effect on retinal cells in experimental conditions. [9][10][11][12][13][14][15][16][17][18][19][20][21][22] Particularly for Ginkgo biloba, potential antioxidant functions have been discussed to be helpful for impaired retinal cells such as Mü ller cells.…”

Section: Introductionmentioning

confidence: 99%

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Dosage dependence of the effect of Ginkgo biloba on the rat retinal ganglion cell survival after optic nerve crush

Zhan

et al. 2008

Eye

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Purpose To investigate the dosage dependence of the Ginkgo biloba effect on retinal ganglion cell survival in the rat optic nerve crush model. Methods The study included 56 SpragueDawley rats, the right optic nerve of which was crushed in a standardized manner. Two hours after the crush and once daily during the follow-up, the animals received intragastral applications of saline (saline group; n ¼ 13), or of a G. biloba extract of 0.25% concentration (n ¼ 14; low-dosage group), 1% concentration (n ¼ 15; medium-dosage group), or 4% concentration (n ¼ 14; high-dosage group). At 23 days after the optic nerve crush, the retinal ganglion cells were retrogradely labelled by injecting 3% fluorogold into the superior colliculi of the brain. At 4 weeks after baseline, the animals were killed. Retinal flat mount photographs were assessed for number and density of the retinal ganglion cells. Results The mean survival rate defined as the ratio of retinal ganglion cell density in the right eye with optic nerve crash divided by the retinal ganglion cell density in left eye without optic nerve intervention increased significantly (Po0.001) from 58.4 ± 9.0% in the saline group to 68.5 ± 5.7% in the low-dosage group, to 73.7 ± 6.4% in the medium-dosage group, and to 74.2 ± 6.8% in the high-dosage group. Conclusions Intragastral applications of a G. biloba extract applied after an experimental and standardized optic nerve crush in rats were associated with a higher survival rate of retinal ganglion cells in a dosage-dependent manner.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dosage dependence of the effect of Ginkgo biloba on the rat retinal ganglion cell survival after optic nerve crush

Zhan

et al. 2008

Eye

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“…In addition, chronic memantine treatment decreased elevated vitreoretinal VEGF protein levels and blood-retinal barrier breakdown in diabetic rats [226]. Recently, Smith et al demonstrated that the s receptor 1 ligand(+)-pentazocine treatment conferred significant neuro protection, reduced evidence of oxidative stress and preserved retinal architecture in diabetic mice [227].…”

Section: Neuroprotectionmentioning

confidence: 99%

Pathophysiology and management of diabetic retinopathy

El‐Asrar¹,

Al-Mezaine

Ola

2009

Expert Review of Ophthalmology

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Diabetic retinopathy remains a major cause of worldwide preventable blindness. In this review, we evaluate the recent advances in understanding the molecular mechanisms of diabetic retinopathy, highlight the current management of diabetic retinopathy and new therapeutic approaches, and discuss the range of potential future therapeutic strategies in order to combat the disease. The microvasculature of the retina responds to hyperglycemia through a number of biochemical changes, including the activation of PKC, increased advanced glycation endproducts formation, polyol pathway and oxidative stress, and activation of the renin-angiotensin system. There is an accumulating body of evidence that inflammation and neurodegeneration play a prominent role in the pathogenesis of diabetic retinopathy. Strict metabolic control, tight blood pressure control, laser photocoagulation and vitrectomy remain the standard care for diabetic retinopathy. Emerging therapies include intravitreal triamcinolone or anti-VEGF agents, ruboxistaurin, renin-angiotensin system blockers, fenofibrate, islet cell transplantation, PPAR-g agonists and intravitreal hyaluronidase. However, more randomized, controlled clinical trials are required to clarify their role alone or in combination. Learning objectivesUpon completion of this activity, participants should be able to:• Identify factors that contribute to the development of diabetic retinopathy Medscape: Continuing Medical Education OnlineThis activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of MedscapeCME and Expert Reviews Ltd. MedscapeCME is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. MedscapeCME designates this educational activity for a maximum of 1.5 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity. All other clinicians completing this activity will be issued a certificate of participation. To participate in this journal CME activity: (1) review the learning objectives and author disclosures; (2) study the education content; (3) take the post-test and/or complete the evaluation at http://cme.medscape.com/CME/expertreviews; (4) view/print certificate. For reprint orders, please contact reprints@expert-reviews.comExpert Rev. Ophthalmol. 4(6), (2009) 628Review Abu El-Asrar, Al-Mezaine & Ola CME Diabetic retinopathy (DR) is the most common microvascular complication of diabetes and remains one of the leading causes of blindness worldwide among adults aged 20-74 years. The two most important visual complications of DR are diabetic macular edema (DME) and proliferative DR (PDR). The prevalence of DR increases with the duration of diabetes, and nearly all people with Type 1 diabetes, and more than 60% of those with Type 2, have some retinopathy after 20 years. In the Wisconsin Epide...

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“…If one considers just the protection of RGCs, a plethora of approaches can be collected from the literature. For example, anti-inflammatory drugs such as nonsteroidal cyclooxygenase inhibitor nepafenac Krady et al, 2005;Vincent and Mohr, 2007); several salicylates (Zhang et al, 2007); the glutamate NMDA receptor antagonist, memantine (Kusari et al, 2007); cannabidiol (CBD) (El-Remessy et al, 2006); NGF (Hammes et al, 1995b); IGF-1 (Seigel et al, 2006); aldose reductase inhibitors (Asnaghi et al, 2003); erythropoietin (EPO) To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print.…”

Section: Experimental Approaches To the Treatment Of Diabetic Retinopmentioning

confidence: 99%

“…Memantine significantly improved amplitudes of ERG a and b waves. Another possible mechanism of the neuroprotective effect of memantine in the retinas of STZ-induced diabetic rats could be the inhibition of retinal type 3 serotonin and nicotinic Ach receptors, although elevated serotonin and acetylcholine levels have not been demonstrated in diabetic retina (Kusari et al, 2007). 4.6.3.6 Nepafenac p1335 Nepafenac is a prodrug of amfenac, a nonsteroidal anti-inflammatory drug that inhibits COX-1 and COX-2 and the synthesis of proinflammatory prostaglandins (Kapin et al, 2003).…”

Section: Calpain Inhibitorsmentioning

confidence: 99%

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Szabadfi

Pintér

Reglődi

et al. 2014

International Review of Cell and Molecular Biology

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Any queries or remarks that have arisen during the processing of your manuscript are listed below and are highlighted by flags in the proof. (AU indicates author queries; ED indicates editor queries; and TS/TY indicates typesetter queries.) Please check your proof carefully and answer all AU queries. Mark all corrections and query answers at the appropriate place in the proof (e.g., by using on-screen annotation in the PDF file http:// www.elsevier.com/book-authors/science-and-technology-book-publishing/overviewof-the-publishing-process) or compile them in a separate list, and tick off below to indicate that you have answered the query. Please return your input as instructed by the project manager. Location in ChapterQuery / remark AU:1, page 47 Please check the change made in the table title. AU:2, page 57 Citation " Frank et al. (1997)" has not been found in the reference list. Please supply full details for this reference. AU:3, page 58Citation "Wang et al. (2004)" has not been found in the reference list. Please supply full details for this reference. AU:4, page 63The citation "Wang et al. (2010)" has been changed to " Wang et al. (2010)" to match the author name/date in the reference list. Please check here and in subsequent occurrences, and correct if necessary. AU:5, page 3The abbreviations IBA-1 and ZFDM are used only once in the text and they have been deleted in the text. Please consider deleting them from the abbreviation list. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:6, page 3Please check if all occurrences of "interstitial cell adhesion molecule 1" should be changed to "intercellular adhesion molecule 1." AU:7, page 3Please check the change from "neural" to "neuronal" to match with the text.AU:8, page 3The abbreviation "PKCa" is not used in the text. Please check and delete from the abbreviation list. AU:9, page 9Please check if "retinal ganglion cells (RGCs)" is okay as edited.AU:10, page 13 Please check the change from "retinal circuity" to "retinal circuitry."AU:11, page 17 Please check if "polyamine catabolism" is okay as edited. AU:20, page 46 Please check if edit to sentence starting "The STZ-induced diabetic. . ." is okay. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:21, page 72Please check if "SST" is okay as edited.AU:2...

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Effect of Memantine on Neuroretinal Function and Retinal Vascular Changes of Streptozotocin-Induced Diabetic Rats

Cited by 114 publications

References 52 publications

Dosage dependence of the effect of Ginkgo biloba on the rat retinal ganglion cell survival after optic nerve crush

Dosage dependence of the effect of Ginkgo biloba on the rat retinal ganglion cell survival after optic nerve crush

Pathophysiology and management of diabetic retinopathy

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

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