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Neuroprotective effect of memantine on hippocampal neurons in infantile rat hydrocephalus
Burak Cabuk1, Volkan Etus, Suheyla Uyar Bozkurt
1Turkish Navy Golcuk Military Hospital, Department of Neurosurgery, Kocaeli, Turkey.
Insights
Memantine treatment protected hippocampal neurons in infantile rats with hydrocephalus, reducing neuronal loss and nitric oxide synthase activity. This suggests memantine offers neuroprotection against hydrocephalus-induced brain injury.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Infantile hydrocephalus can cause significant neuronal damage in the hippocampus.
- Nitric oxide synthase (NOS) activity is implicated in the neurotoxicity associated with hydrocephalus.
Purpose of the Study:
- To investigate the neuroprotective effects of memantine on hippocampal neurons in a rat model of infantile hydrocephalus.
- To assess the impact of memantine on neuronal survival and NOS activity in the hippocampus.
Main Methods:
- Hydrocephalus was induced in Sprague-Dawley rat pups using kaolin injection.
- Rats received daily memantine (20mg/kg) or a placebo for two weeks post-induction.
- Immunohistochemistry and neuronal quantification were performed on hippocampal tissues.
Main Results:
- Hydrocephalus led to significant neuronal loss and increased NOS immunoreactivity in the hippocampus.
- Memantine treatment preserved significantly more neurons, particularly in CA1 and CA2 regions.
- Memantine also reduced NOS immunoreactivity in the CA1 and CA2 hippocampal subregions.
Conclusions:
- Hippocampal neurons are vulnerable to injury in experimental infantile hydrocephalus.
- Early memantine administration demonstrates a neuroprotective effect against hydrocephalus-induced hippocampal damage.
- Memantine may be a potential therapeutic agent for mitigating excitotoxic injury in infantile hydrocephalus.
Aim:
The effect of memantine administration on hippocampal neurons of the infantile rats with kaolin induced hydrocephalus was investigated.
Material And Methods:
Hydrocephalus was induced by injecting kaolin into the cisterna magna of 3-weeks old Sprague-Dawley rat pups. One group received a single daily dose of 20mg/kg memantine i.p. following hydrocephalus induction for a period of two weeks. By the end of the two-week period, animals were radiologically evaluated by magnetic resonance imaging and then sacrificed to get their cerebrums removed. Both immunohistochemical analysis of nitric oxide synthase activity and quantification of spared neurons in CA1, CA2 and CA3 regions of hippocampus were performed.
Results:
In hydrocephalus-induced rats considerable neuronal loss associated with significantly increased nitric oxide synthase immunoreactivity were determined in all hippocampal regions. However, memantine treated rats showed significantly higher number of spared neuron counts and reduced nitric oxide synthase immunoreactivity in CA1 and CA2 regions compared with the non-treated rats.
Conclusion:
The findings of the study show that hippocampal neurons may constitute important targets for injury secondary to hydrocephalic process in experimental infantile hydrocephalus. Early anti-excitotoxic treatment with memantine seems to have a neuroprotective effect especially in the CA1 and CA2 subunits of the hippocampus.
