AI Article Synopsis
- Subarachnoid hemorrhage (SAH) causes brain injury through glutamate excitotoxicity and excessive calcium influx, triggering apoptosis.
- A study using a rat model investigated memantine's neuro-protective effects post-SAH, focusing on neuro-behavioral improvement and neuronal cell preservation.
- Results showed that memantine reduced oxidative stress, preserved blood-brain barrier integrity, and enhanced neurological outcomes, suggesting its potential for treating SAH-induced brain damage.
Article Abstract
Subarachnoid hemorrhage (SAH) causes brain injury via glutamate excitotoxicity, which leads to an excessive Ca(2+) influx and this starts an apoptotic cascade. Memantine has been proven to reduce brain injury in several types of brain insults. This study investigated the neuro-protective potential of memantine after SAH and explored the underlying mechanisms. An endovascular perforation rat model of SAH was used and Sprague-Dawley rats were randomized into sham surgery, SAH + vehicle, and SAH + memantine groups. The effects of memantine on SAH were evaluated by assessing the neuro-behavioral functions, blood-brain barrier (BBB) permeability and neuronal cell preservation. The mechanisms of action of memantine, with its N-methyl-D-aspartate (NMDA) antagonistic characteristics on nitric oxide synthase (NOS) expression and peroxynitrite formation, were also investigated. The apoptotic cascade after SAH was suppressed by memantine. Neuronal NOS (nNOS) expression, peroxynitrite formation, and subsequent oxidative/nitrosative stress were also reduced. Memantine effectively preserved BBB integrity, rescued neuronal injury, and improved neurological outcome in experimental SAH. Memantine has neuro-protective potential in experimental SAH and may help combat SAH-induced brain damage in the future.
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| http://dx.doi.org/10.1007/s12035-014-8767-9 | DOI Listing |
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