By Marianne Renner, Antoine Triller (auth.), Dennis J. Selkoe, Antoine Triller, Yves Christen (eds.)
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Additional resources for Synaptic Plasticity and the Mechanism of Alzheimer's Disease
J Cell Sci 119:4866–4877. Hayashi Y, Shi SH, Esteban JA, Piccini A, Poncer JC, Malinow R (2000) Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction. Science 287:2262–2267. Hebb DO (1949) Organization of behavior (New York, Wiley). Hering H, Sheng M (2001) Dendritic spines: structure, dynamics and regulation. Nature Rev Neurosci 2:880–888. Hollmann M, Heinemann S (1994) Cloned glutamate receptors. Annu Rev Neurosci 17:31–108. 1 family: organizers of the membrane and cytoskeleton.
1995). Although this adult plasticity is thought to depend on changes in the strength of established synaptic connections (Hebb 1949), it could also involve structural alterations, including synapse formation and elimination (Antonini and Stryker 1993; Chklovskii et al. 2004; Knott et al. 2002; Lowel and Singer 1992; Ramon y Cajal 1893; Stepanyants et al. 2002; Turner and Greenough 1985; Ziv and Smith 1996). To address this possibility, we have focused our recent studies on dendritic spines and axonal boutons, the sites where the majority of excitatory synapses are found and, therefore, potential substrates for structural plasticity of cortical circuits.
1994) or GluR4 (Zhu et al. 2000) subunits are added into synapses in an activity-dependent manner during synaptic plasticity. This regulated pathway is triggered transiently upon induction of LTP and results in a net increase in the number of AMPARs present at synapses (Malinow et al. 2000). The synaptic delivery of GluR1 is also regulated by physiological stimulation in living animals, as it has been reported for neocortical neurons upon sensory stimulation (Takahashi et al. 2003) and in the lateral amygdala after fear conditioning (Rumpel et al.