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Aspirin increases NMDA receptor subunit 2A concentrations in rat hippocampus

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dc.creator ERSOY, Ismail Hakki
dc.creator ŞENOL, Altuğ
dc.creator ACARTÜRK, Gursel
dc.creator ŞENOL, Nilgün
dc.creator CEYHAN, Betul Mermi
dc.creator SÜTÇÜ, Recep
dc.date 2012-01-31T22:00:00Z
dc.date.accessioned 2020-10-06T12:03:32Z
dc.date.available 2020-10-06T12:03:32Z
dc.identifier fd95c97b-bb76-4297-89c3-45addf455a1d
dc.identifier 10.3109/10799893.2011.641975
dc.identifier https://avesis.sdu.edu.tr/publication/details/fd95c97b-bb76-4297-89c3-45addf455a1d/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/77088
dc.description The N-methyl-d-aspartate receptor (NMDAR), a heteromeric protein, is a glutamate receptor that has three classes of subunits: NR1, NR2, and NR3. It has been reported that these receptors are involved in synaptogenesis, synaptic plasticity, and many other processes in the central nervous system. The aim of this study is to investigate the efficacy of aspirin on hippocampal NMDARs. Sixteen rats were studied in two groups, with eight animals in each group. The first group was the control group, and the second one was the aspirin-given group. Aspirin (acetylsalicylic acid) was administered orally to the rats (200 mg/kg). Tissue samples were obtained after 3 h. The brain was removed, and both hippocampi were dissected out for evaluation. It was found that acute doses of aspirin caused increases on the levels of NMDAR 2A (NR2A) receptors and malondialdehyde (MDA), the end product of lipid peroxidation. Production was significantly increased in the aspirin-given group. We know that MDA is a marker for free radical-mediated tissue damage. In conclusion, lipid peroxidation, caused by acute doses of aspirin may lead to excitotoxicity effects by a hippocampal NR2A-mediated mechanism.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Aspirin increases NMDA receptor subunit 2A concentrations in rat hippocampus
dc.type info:eu-repo/semantics/article


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