Aspirin increases NMDA receptor subunit 2A concentrations in rat hippocampus

Authors: Senol, Nilgun1; Ceyhan, Betul Mermi2; Ersoy, Ismail Hakki3; Senol, Altug3; Acarturk, Gursel3; Sutcu, Recep2

Source: Journal of Receptors and Signal Transduction, Volume 32, Number 1, February 2012 , pp. 17-21(5)

Publisher: Informa Healthcare

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Abstract:

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.

Keywords: Malondialdehyde; lipid peroxidation; glutamate receptors; acetylsalicylic acid

Document Type: Research article

DOI: http://dx.doi.org/10.3109/10799893.2011.641975

Affiliations: 1: 1Department of Neurosurgery, Suleyman Demirel University School of Medicine, Isparta, Turkey 2: 2Department of Biochemistry and Physiology, Suleyman Demirel University School of Medicine, Isparta, Turkey 3: 3Department of Internal Medicine, Suleyman Demirel University School of Medicine, Isparta, Turkey

Publication date: 2012-02-01

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