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Functional protective effects of long-term memantine treatment in the DBA/2J mouse
Jenny Atorf1, Michael Scholz, Fabian Garreis
1Department of Ophthalmology, University Hospital Erlangen, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
Purpose:
To analyse the effects of long-term memantine treatment on the retinal physiology and morphology of DBA/2J mice.
Methods:
DBA/2J (D2J) mice received i.p. injections of the NMDA receptor antagonist memantine, which protects neurons from abnormally elevated glutamate levels, twice a day over a period of 7 months. At the age of 2, 6 and 10 months, the intraocular pressure (IOP) and electroretinograms (ERGs) were measured in all treated D2J mice, in untreated D2J controls and in C57Bl/6 (B6) wild-type mice. After the last measurement at the age of 10 months, the mice were killed and the retinae and the optic nerves were analysed morphologically.
Results:
The IOP increased with age in both D2J and B6 mice with a larger increase in the D2J strain. IOPs were not influenced by memantine treatment. The response amplitude of the scotopic flash ERG decreased with age in the D2J strain. This amplitude decrease, particularly that of the b-wave, was smaller in treated D2J mice. The retinae of treated D2J mice exhibited less peripheral degeneration of cone photoreceptors, and optic nerve neuropathy was less frequent.
Conclusions:
Application of the NMDA receptor antagonist memantine diminished retinal neurodegeneration in the D2J mice and had a protective effect on the b-wave amplitude of the scotopic flash ERG. This protection may occur secondarily as memantine primarily acts on retinal ganglion cells.
Insights
Long-term memantine treatment protected DBA/2J mice from retinal neurodegeneration and preserved scotopic flash electroretinogram (ERG) b-wave amplitude. This NMDA receptor antagonist showed a protective effect on retinal ganglion cells.
Area of Science:
- Neuroscience
- Ophthalmology
- Pharmacology
Background:
- DBA/2J mice are a model for age-related glaucoma and retinal degeneration.
- Elevated glutamate levels can cause excitotoxicity and neuronal damage in the retina.
- Memantine is an NMDA receptor antagonist used to treat Alzheimer's disease.
Purpose of the Study:
- To investigate the long-term effects of memantine on retinal physiology and morphology in DBA/2J mice.
- To assess memantine's impact on intraocular pressure (IOP) and electroretinograms (ERGs).
- To evaluate memantine's neuroprotective potential against retinal degeneration in a glaucoma mouse model.
Main Methods:
- DBA/2J mice received twice-daily intraperitoneal injections of memantine for 7 months.
- Intraocular pressure (IOP) and electroretinograms (ERGs) were measured at 2, 6, and 10 months of age.
- Retinal and optic nerve morphology were analyzed post-mortem at 10 months.
Main Results:
- Memantine did not influence intraocular pressure (IOP) in DBA/2J mice.
- The age-related decrease in scotopic flash electroretinogram (ERG) b-wave amplitude was attenuated in memantine-treated mice.
- Treated mice showed reduced peripheral cone photoreceptor degeneration and less frequent optic nerve neuropathy.
Conclusions:
- Memantine administration diminished retinal neurodegeneration in DBA/2J mice.
- Memantine exerted a protective effect on the b-wave amplitude of the scotopic flash ERG.
- The neuroprotective effects may be secondary to memantine's primary action on retinal ganglion cells.
