Related Experiment Video
Updated: Aug 13, 2026

In vivo Imaging of Optic Nerve Fiber Integrity by Contrast-Enhanced MRI in Mice
Published on: July 22, 2014
Memantine reduces alterations to the mammalian retina, in situ, induced by ischemia
1Nuffield Laboratory of Ophthalmology, University of Oxford, UK.
Abstract:
The aim of the study was to determine whether memantine could slow down the changes seen in the rabbit and rat retina following ischemia/reperfusion. A "suction cup procedure," which raises the intraocular pressure, was used to give an ischemic insult to the rabbit retina. The electroretinogram was recorded before ischemia and after 2 days of reperfusion. Memantine or saline (10 microl) was injected into the eye before ischemia. Immunohistochemistry was used to study the effect of ischemia/reperfusion on the GABA, ChAT, and alphaPKC immunoreactivities. Ischemia/reperfusion injury to the rat retina was induced by raising the intraocular pressure above the systolic blood pressure for 60 min, followed by reperfusion of 3-14 days. Memantine (5 mg/kg) or saline was injected i.p. at the onset of ischemia or reperfusion. Immunohistochemistry was used to study the effect of ischemia/reperfusion on the ChAT, alphaPKC, and Thy-1 immunoreactivities. In addition, morphometric analysis was carried out to determine the effects of ischemia/reperfusion on the thickness of the retina. Ischemia for 75 min caused a change in the nature of the normal GABA and ChAT immunoreactivities in the rabbit retina and a reduction in the b-wave of the electroretinogram. When memantine was injected into the vitreous humour at the onset of an ischemic insult, the changes in the GABA and ChAT immunoreactivities were reduced and the recovery of the reduced b-wave of the electroretinogram after 2 days reperfusion was enhanced significantly. Ischemia for 60 min followed by 3 days reperfusion showed a clear change in ChAT immunoreactivity in the rat retina. The Thy-1 immunoreactivity was only clearly altered after a reperfusion period of 7 days. Moreover, a measurable change in the thickness of the inner retinal layers was detected after 14 days of reperfusion. When given at the onset of ischemia, memantine counteracted the effect of ischemia/reperfusion to varying degrees. However, when memantine was given at the onset of the reperfusion this was not the case. The combined data show that a single injection of memantine given i.p. or intravitreally will protect the retina from a subsequent ischemic insult.
Insights
Memantine protects the retina from ischemia/reperfusion injury. This study shows memantine injections, given before or during ischemia, significantly reduce retinal damage and improve recovery in animal models.
Area of Science:
- Ophthalmology
- Neuroscience
- Pharmacology
Background:
- Retinal ischemia/reperfusion (I/R) injury is a significant cause of vision loss.
- Understanding protective mechanisms against I/R injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the neuroprotective potential of memantine against retinal I/R injury in rabbit and rat models.
- To evaluate the impact of memantine on specific retinal biomarkers and structural integrity following I/R.
Main Methods:
- Induction of retinal I/R injury using a suction cup procedure (rabbits) or elevated intraocular pressure (rats).
- Administration of memantine via intravitreal injection (rabbits) or intraperitoneal injection (rats) at different time points.
- Assessment of retinal function using electroretinography (ERG) and evaluation of protein expression (GABA, ChAT, alphaPKC, Thy-1) and retinal thickness via immunohistochemistry and morphometric analysis.
Main Results:
- Ischemia/reperfusion caused significant changes in GABA and ChAT immunoreactivity and reduced ERG b-wave amplitude in rabbits.
- Memantine administered before ischemia significantly reduced these changes and enhanced ERG recovery in rabbits.
- In rats, ischemia/reperfusion altered ChAT and Thy-1 immunoreactivity and retinal thickness; memantine was protective when given at ischemia onset but not at reperfusion onset.
Conclusions:
- Memantine demonstrates significant neuroprotective effects against retinal ischemia/reperfusion injury in both rabbit and rat models.
- Timing of memantine administration is critical, with pre-ischemic or early ischemic treatment being most effective.
- These findings suggest memantine as a potential therapeutic agent for preventing or mitigating retinal damage caused by ischemic events.

