title: Pre-treatment with vinpocetine protects against retinal ischemia.
abstract: Vinpocetine has been shown to have beneficial effects for tissues of the central nervous system subjected to ischemia and other related metabolic insults. We recently showed vinpocetine promotes glucose availability, prevents unregulated cation channel permeability and regulates glial reactivity when present during retinal ischemia. Less is known however about the ability of vinpocetine to protect against future ischemic insults. This study explores the effect of vinpocetine when used as a pre-treatment in an ex vivo model for retinal ischemia using cation channel permeability of agmatine (AGB) combined with immunohistochemistry as a measure for cell functionality. We found that vinpocetine pre-treatment reduced cation channel permeability and apoptotic marker immunoreactivity in the GCL and increased parvalbumin immunoreactivity of inner retinal neurons in the inner nuclear layer following ischemic insult. Vinpocetine pre-treatment also reduced Müller cell reactivity following ischemic insults of up to 120 min compared to untreated controls. Many of vinpocetine's effects however were transient in nature suggesting the drug can protect retinal neurons against future ischemic damage but may have limited long-term applications.
authors.affiliation: Centre for Eye Health, University of New South Wales, Sydney, 2052, Australia; School of Optometry and Vision Science, University of New South Wales, Sydney, 2052, Australia. Electronic address: l.nivison-smith@unsw.edu.au.
authors.forename: Lisa
authors.initials: L
authors.lastname: Nivison-Smith
authors.affiliation: School of Optometry and Vision Science, University of New South Wales, Sydney, 2052, Australia.
authors.forename: Pauline
authors.initials: P
authors.lastname: Khoo
authors.affiliation: School of Optometry and Vision Science, University of Auckland, New Zealand; New Zealand National Eye Centre, University of Auckland, New Zealand.
authors.forename: Monica L
authors.initials: ML
authors.lastname: Acosta
authors.affiliation: Centre for Eye Health, University of New South Wales, Sydney, 2052, Australia; School of Optometry and Vision Science, University of New South Wales, Sydney, 2052, Australia; School of Optometry and Vision Science, University of Auckland, New Zealand; New Zealand National Eye Centre, University of Auckland, New Zealand.
authors.forename: Michael
authors.initials: M
authors.lastname: Kalloniatis
mesh_terms: D000818:Animals; D064032:Calbindin 2 / Q000378:metabolism; D002121:Calcium Channel Blockers; D004195:Disease Models, Animal; D063928:Ependymoglial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D007511:Ischemia / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D018613:Microscopy, Confocal; D018696:Neuroprotective Agents / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D012164:Retinal Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D055351:Retinal Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D014748:Vinca Alkaloids / Q000494:pharmacology*
chemical_list: D064032:Calbindin 2; D002121:Calcium Channel Blockers; D018696:Neuroprotective Agents; D014748:Vinca Alkaloids; C013983:vinpocetine
keywords: AGB; Cation channel; Retinal ischemia; Vinpocetine