Impact of Beta Amyloid on Excitatory Synaptic Transmission and Plasticity
Chapter
Abstract
There is a keen interest in identifying the effects of Aβ on synapses. Here we review some of the published work on its effects on excitatory synaptic transmission and plasticity. We also provide new information indicating that activity-induced release of Aβ from either pre- or postsynaptic neurons can block structural plasticity.
Keywords
Synaptic Transmission Amyloid Precursor Protein Synaptic Function Structural Plasticity Synaptic Depression
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Preview
Unable to display preview. Download preview PDF.
References
- Bliss TV, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361:31–39.PubMedCrossRefGoogle Scholar
- Buxbaum JD, Thinakaran G, Koliatsos V, O’Callahan J, Slunt HH, Price DL, Sisodia SS (1998) Alzheimer amyloid protein precursor in the rat hippocampus: transport and processing through the perforant path. J Neurosci 18:9629–9637.PubMedGoogle Scholar
- Chapman PF, White GL, Jones MW, Cooper-Blacketer D, Marshall VJ, Irizarry M, Younkin L, Good MA, Bliss TV, Hyman BT, Younkin SG, Hsiao KK (1999) Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nature Neurosci 2:271–276.PubMedCrossRefGoogle Scholar
- Chen QS, Wei WZ, Shimahara T, Xie CW (2002) Alzheimer amyloid beta-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus. Neurobiol Learn Mem 77:354–371.PubMedCrossRefGoogle Scholar
- Cullen WK, Suh YH, Anwyl R, Rowan MJ (1997) Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments. Neuroreport 8:3213–3217.PubMedGoogle Scholar
- Hardy J, Selkoe DJ (2002) The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 297:353–356.PubMedCrossRefGoogle Scholar
- Hsia AY, Masliah E, McConlogue L, Yu GQ, Tatsuno G, Hu K, Kholodenko D, Malenka RC, Nicoll RA, Mucke L (1999) Plaque-independent disruption of neural circuits in Alzheimer’s disease mouse models. Proc Natl Acad Sci USA 96:3228–3233.PubMedCrossRefGoogle Scholar
- Hsieh H, Boehm J, Sato C, Iwatsubo T, Tomita T, Sisodia S, Malinow R (2006) AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss. Neuron 52:831–843.PubMedCrossRefGoogle Scholar
- Kamenetz F, Tomita T, Hsieh H, Seabrook G, Borchelt D, Iwatsubo T, Sisodia S, Malinow R (2003) APP processing and synaptic function. Neuron 37:925–937.PubMedCrossRefGoogle Scholar
- Kopec CD, Li B, Wei W, Boehm J, Malinow R (2006) Glutamate receptor exocytosis and spine enlargement during chemically induced long-term potentiation. J Neurosci 26:2000–2009.PubMedCrossRefGoogle Scholar
- Lambert MP, Barlow AK, Chromy BA, Edwards C, Freed R, Liosatos M, Morgan TE, Rozovsky I, Trommer B, Viola KL, Wals P, Zhang C, Finch CE, Krafft GA, Klein WL (1998) Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 95:6448–6453.PubMedCrossRefGoogle Scholar
- Larson J, Lynch G, Games D, Seubert P (1999) Alterations in synaptic transmission and long-term potentiation in hippocampal slices from young and aged PDAPP mice. Brain Res 840:23–35.PubMedCrossRefGoogle Scholar
- Lazarov O, Lee M, Peterson DA, Sisodia SS (2002) Evidence that synaptically released beta-amyloid accumulates as extracellular deposits in the hippocampus of transgenic mice. J Neurosci 22:9785–9793.PubMedGoogle Scholar
- Moechars D, Dewachter I, Lorent K, Reverse D, Baekelandt V, Naidu A, Tesseur I, Spittaels K,Haute CV, Checler F, Godaux E, Cordell B, Van Leuven F (1999) Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. J Biol Chem 274:6483–6492.PubMedCrossRefGoogle Scholar
- Molnar Z, Soos K, Lengyel I, Penke B, Szegedi V, Budai D (2004) Enhancement of NMDA responses by beta-amyloid peptides in the hippocampus in vivo. Neuroreport 15:1649–1652.PubMedCrossRefGoogle Scholar
- Morishita W, Marie H, Malenka RC (2005) Distinct triggering and expression mechanisms underlie LTD of AMPA and NMDA synaptic responses. Nature Neurosci 8:1043–1050.PubMedCrossRefGoogle Scholar
- Selkoe DJ (2001) Alzheimer’s disease: genes, proteins, and therapy. Physiol Rev 81(2):741–766.PubMedGoogle Scholar
- Snyder EM, Nong Y, Almeida CG, Paul S, Moran T, Choi EY, Nairn AC, Salter MW, Lombroso PJ, Gouras GK, Greengard P (2005) Regulation of NMDA receptor trafficking by amyloid-beta. Nature Neurosci 8:1051–1058.PubMedCrossRefGoogle Scholar
- Stern EA, Bacskai BJ, Hickey GA, Attenello FJ, Lombardo JA, Hyman BT (2004) Cortical synaptic integration in vivo is disrupted by amyloid-beta plaques. J Neurosci 24:4535–4540.PubMedCrossRefGoogle Scholar
- Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, Hansen LA, Katzman R (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580.PubMedCrossRefGoogle Scholar
- Walsh DM, Klyubin I, Fadeeva JV, Cullen WK, Anwyl R, Wolfe MS, Rowan MJ, Selkoe DJ (2002) Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature 416:535–539.PubMedCrossRefGoogle Scholar
- Wang Q, Rowan MJ, Anwyl R (2004) Beta-amyloid-mediated inhibition of NMDA receptor-dependent long-term potentiation induction involves activation of microglia and stimulation of inducible nitric oxide synthase and superoxide. J Neurosci 24:6049–6056.PubMedCrossRefGoogle Scholar
- Wu J, Anwyl R, Rowan MJ (1995) beta-Amyloid selectively augments NMDA receptor-mediated synaptic transmission in rat hippocampus. Neuroreport 6:2409–2413.PubMedCrossRefGoogle Scholar
Copyright information
© Springer-Verlag Berlin Heidelberg 2008