Welcome to visit Acta Anatomica Sinica! Today is
Chinese






β-amyloid protein induces the changes of astrocytic N-methyl-D-aspartate receptor subunits expression in rat hippocampus
GAO Xiang-hong SONG Yi-zhi CHANG Li-rong ZHANG Ya-li WU Yan*
Acta Anatomica Sinica ›› 2013, Vol. 44 ›› Issue (2) : 146-151.
β-amyloid protein induces the changes of astrocytic N-methyl-D-aspartate receptor subunits expression in rat hippocampus
Objective To investigate the effects of β-amyloid protein (Aβ25-35) on astrocytic N-methyl-D-aspartate receptor (NMDAR) subunits in the rat hippocampus. Methods Aβ25-35 (10μmol/L) was added into the primary cultured hippocampal cells for 1 hour and 24 hours. Immunofluorescence technique was applied to investigate the changes of the expression of NR1, NR2A and NR2B between the control group and Aβ groups ( n =10). Results NR1, NR2A and NR2B were expressed in the hippocampal astrocytes.The positive puncta were mainly distributed in the soma and process. The expression was intensive in the soma and scattered in the process. Their expression was increased following Aβ25-35treatment ( P <0.05 vs control group). The expression of NR2A and NR2B were significantly increased ( P <0.05) between Aβ 1hour group and Aβ 24hours group, while there was no significant changes in NR1 group. Conclusion The rat hippocampal astrocytes express NMDAR subunits (NR1, NR2A and NR2B), and their expressions are significantly increased after Aβ25-35treatment, while the variation tendency of NR1 is different from the changes of NR2A and NR2B.
N-methyl-D-aspartate receptor / Astrocyte / β-Amyloid protein / Hippocampus / Immunofluorescence / Rat
[1] Roselli F, Tirard M, Lu J, et al. Soluble β-amylaid1-40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses[J]. J Neurosci, 2005, 25(48):11061-11070.
[2] Lee MC, Ting KK, Adams S, et al. Characterisation of the expression of NMDA receptors in human astrocytes[J]. PLoS One, 2010, 5(11):e14123.
[3] Zhou Y, Li HL, Zhao R, et al. Astrocytes express N-methyl-D-aspartate receptor subunits in development,ischemia and post-ischemia[J]. Neurochem Res, 2010, 35(12):2124-2134.
[4] Verkhratsky A, Kirchhoff F. NMDA receptors in glia[J]. Neuroscientist, 2007, 13(1):28-37.
[5] Luque JM, Richards JG. Expression of NMDA 2B receptor subunit mRNA in Bergmann glia[J]. Glia, 1995, 13(3):228-232.
[6] Karadottir R, Cavelier P, Bergersen LH, et al. NMDA receptors are expressed in oligodendrocytes and activated in ischaemia[J]. Nature, 2005, 438(7071):1162-1166.
[7] Salter MG, Fern R. NMDA receptors are expressed in developing oligodendrocyte processes and mediate injury[J]. Nature, 2005, 438(7071):1167-1171.
[8] Seifert G, Steinhauser C. Glial cells in the mouse hippocampus express AMPA receptors with an intermediateCa2 + permeability[J]. Eur J Neurosci,1995, 7(9):1872-1881.
[9] Krebs C, Fernandes HB, Sheldon C, et al. Functional NMDA receptor subtype 2B is expressed in astrocytes after ischemia in vivo and anoxia in vitro[J]. J Neurosci, 2003, 23(8):3364-3372.
[10] Zhang X, Zhang J, Chen C. Long-term potentiation at hippocampal perforant path-dentate astrocyte synapses[J]. Biochem Biophys Res Commun, 2009, 383(3):326-330.
[11] Shirotain K, Tsubuki S, Iwata N, et al. Neprilysin degrades both amyloid beta peptides 1-40 and 1-42 most rapide and efficiently among thiorphan and phosphoramidon sensitive endopeptidases[J]. J Biol Chem, 2001, 276(24):21895-21901.
[12] De Felice FG, Velasco PT, Lambert MP, et al. Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine[J].J Biol Chem, 2007, 282(15):11590-11601
[13] Kiedrowski L. Critical role of sodium in cytosolic[Ca 2+]elevations in cultured hippocampal CA1 neurons during anoxic depolarization[J]J Neurochem, 2007,100(4):915-923
[14] Liu JP, Gao XL, Wu Y. N-methyl-D-aspartate receptors mediate excitotoxicity in amyloid beta-induced synaptic pathology of Alzheimer’s disease[J]. Neuroembryol Aging, 2008, 5(4):134-143.
[15] Perea G, Araque A. GLIA modulates synaptic transmission[J]. Brain Res Rev, 2010, 63(12): 93-102.
[16] Allen NG, Barres BA. Signaling between glia and neurons: focus on synaptic plasticity[J]. Curr Opin Neurobiol, 2005, 15(5):542-548.
[17] Domenici MR, Paradisi S, Sacchetti B, et al. The presence of astrocytes enhances beta amyloid-induced neurotoxicity in hippocampal cell cultures[J]. J Physiol Paris, 2002, 96(3-4):313-316.
[18] Thal DR. The role of astrocytes in amyloid β-protein toxicity and clearance[J]. Exp Neurol, 2012, 236(1):1-5.
[19] Nagele RG, D′Andrea MR, Lee H, et al. Astrocytes accumulate a beta 42 and give rise to astrocytic amyloid plaques in Alzheimer disease brains[J]. Brain Res, 2003, 971(2):197-209.
[20] Texido L, Martin-Satue M, Alberdi E, et al. Amyloid-peptide oligomers directly activate NMDA receptors[J]. Cell Calcium, 2011, 49(3):184-190.
[21] Low CM, Wee KS. New insights into the not-so-new NR3 subunits of N-methyl-D-aspartate receptor: localization, structure, and function[J]. Mol Pharmacol, 2010, 78(1):1-11.
[22] Nakanishi N, Tu S, Shin Y, et al. Neuroprotection by the NR3A subunit of the NMDA receptor[J].J Neurosci, 2009, 29(16):5260-5265.
/
〈 |
|
〉 |