Synaptic AMPA Receptor Plasticity and Behavior

By H. Kessels, R. Malinow. Neuron, 2009

1,036 citations recorded by the source corpus.

The ability to change behavior likely depends on the selective strengthening and weakening of brain synapses. The cellular models of synaptic plasticity, long-term potentiation (LTP) and depression (LTD) of synaptic strength, can be expressed by the synaptic insertion or removal of AMPA receptors (AMPARs), respectively. We here present an overview of studies that have used animal models to show that such AMPAR trafficking underlies several experience-driven phenomena—from neuronal circuit formation to the modification of behavior. We argue that monitoring and manipulating synaptic AMPAR trafficking represents an attractive means to study cognitive function and dysfunction in animal models.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/fc66f8a1388730dc96c553131f87a020f4502d8e

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In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

Citations in the corpus

Modeling the dynamic interaction of Hebbian and homeostatic plasticity. (2014, neutral): “These slots are created by PSD structural proteins (Huganir and Nicoll, 2013; Kessels and Malinow, 2009), some of which play roles in homeostatic plasticity (Shin et al., 2012; Steinmetz and Turrigiano, 2010; Sun and Turrigiano, 2011).”
Neurotoxicity of amyloid β-protein: synaptic and network dysfunction. (2012, background): “2011) or did not (Kessels and Malinow 2009; Balducci et al. 2010; Calella et al. 2010; Cisse et al. 2011b) prevent Ab-induced neuronal dysfunction, leaving the functional significance of an Ab/PrPc interaction uncertain at this writing.”
Sleep and the Price of Plasticity: From Synaptic and Cellular Homeostasis to Memory Consolidation and Integration (2014, background): “GluA2-containing AMPARs are strongly involved in constitutive receptor cycling and synaptic depression, while GluA1-containing AMPARs are linked to synaptic potentiation (Kessels and Malinow, 2009).”
Regulation of AMPA Receptor Trafficking and Synaptic Plasticity (2012, background): “Enhanced receptor exocytosis and recycling occur during synaptic potentiation, while increased rate of endocytosis results in LTD [1,4].”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “This plasticity has been the most widely studied form of LTP and has been posited as a cellular correlate underlying learning and memory (Kessels and Malinow, 2009).”
The restless engram: consolidations never end. (2012, background): “This Ca signal can activate awide range of signaling pathways including CaMKII, PKC, PKA, and MAPK that have each been implicated in the induction of LTP as well as in its later stabilization (Malenka and Bear, 2004; Huang et al., 2013; Kerchner and Nicoll, 2008; Kessels and Malinow, 2009; Lisman et”
The molecular and systems biology of memory. (2014, neutral): “This Ca signal can activate awide range of signaling pathways including CaMKII, PKC, PKA, and MAPK that have each been implicated in the induction of LTP as well as in its later stabilization (Malenka and Bear, 2004; Huang et al., 2013; Kerchner and Nicoll, 2008; Kessels and Malinow, 2009; Lisman et”
Endocytosis, Signaling, and Beyond (2014, background): “…or strength of excitatory neurotransmission is subject to exquisite regulation through endocytosis and recycling of critical postsynaptic signaling receptors that reduce or increase, respectively, synaptic strength and thereby impact learning (Luscher et al. 1999; Kessels and Malinow 2009).”
The Angelman Syndrome-associated ubiquitin ligase Ube3A regulates synapse development by ubiquitinating Arc (2010, neutral): “We focused on the GluR1 subunit of the AMPA receptor, as GluR1 insertion into the plasma membrane is regulated by neuronal activity and by Arc (Newpher and Ehlers, 2008; Kessels and Malinow, 2009; Rial Verde et al., 2006; Shepherd et al., 2006).”