Cross-modal synaptic plasticity in adult primary sensory cortices

Lee, Hey Kyoung; Whitt, Jessica L.

doi:10.1016/j.conb.2015.08.002

Cited by 86 publications

(63 citation statements)

References 59 publications

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“…Synaptic scaling is also observed in vivo (Desai et al, 2002; Diering et al, 2017; Hengen et al, 2016; Lee and Whitt, 2015). A wide range of intracellular and extracellular molecules and signaling pathways regulate homeostatic scaling.…”

Section: Introductionmentioning

confidence: 88%

Neuropilin-2/PlexinA3 Receptors Associate with GluA1 and Mediate Sema3F-Dependent Homeostatic Scaling in Cortical Neurons

Wang

Chiu

Koropouli

et al. 2017

Neuron

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SUMMARY Regulation of AMPA-type glutamate receptor (AMPAR) number at synapses is a major mechanism for controlling synaptic strength during homeostatic scaling in response to global changes in neural activity. We show that the secreted guidance cue semaphorin 3F (Sema3F) and its neuropilin-2 (Npn-2)/plexinA3 (PlexA3) holoreceptor mediate homeostatic plasticity in cortical neurons. Sema3F-Npn-2/PlexA3 signaling is essential for cell surface AMPAR homeostatic downscaling in response to an increase in neuronal activity, Npn-2 associates with AMPARs, and Sema3F regulates this interaction. Therefore, Sema3F-Npn-2/PlexA3 signaling controls both synapse development and synaptic plasticity.

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Section: Introductionmentioning

confidence: 88%

Neuropilin-2/PlexinA3 Receptors Associate with GluA1 and Mediate Sema3F-Dependent Homeostatic Scaling in Cortical Neurons

Wang

Chiu

Koropouli

et al. 2017

Neuron

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“…Homeostatic plasticity is thought to be particularly important during development and during periods of heightened plasticity, triggered by prolonged changes in the sensory environment or by neurological conditions [reviewed in (Turrigiano and Nelson ; Small ; Turrigiano ; Wondolowski and Dickman ; Whitt et al . ; Lee and Whitt )], when there are important activity‐dependent changes in neuronal circuits and remodeling in synaptic contacts. Homeostatic synaptic plasticity has been observed in vivo in different preparations, and proposed to be involved in activity‐dependent refinement of connectivity.…”

Section: In Vivo Homeostatic Synaptic Plasticitymentioning

confidence: 99%

Mechanisms of homeostatic plasticity in the excitatory synapse

Fernandes

Carvalho

2016

Journal of Neurochemistry

131

115

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Brain development, sensory information processing, and learning and memory processes depend on Hebbian forms of synaptic plasticity, and on the remodeling and pruning of synaptic connections. Neurons in networks implicated in these processes carry out their functions while facing constant perturbation; homeostatic responses are therefore required to maintain neuronal activity within functional ranges for proper brain function. Here, we will review in vitro and in vivo studies demonstrating that several mechanisms underlie homeostatic plasticity of excitatory synapses, and identifying participant molecular players. Emerging evidence suggests a link between disrupted homeostatic synaptic plasticity and neuropsychiatric and neurologic disorders. Keywords: AMPA receptors, experience-dependent plasticity, Hebbian synaptic plasticity, homeostatic synaptic plasticity, synapse, synaptic scaling.This article is part of a mini review series: "Synaptic Function and Dysfunction in Brain Diseases". Hebbian and homeostatic synaptic plasticityLearning and memory as well as other forms of human behavior possibly rely on the ability of the mammalian brain to undergo experience-based adaptations in synaptic strength, which becomes stronger or weaker in response to specific patterns of activity. Hebbian synaptic plasticity is the most widely studied form of long-lasting activity-dependent changes in synaptic strength and includes both long-term potentiation (LTP) and its counterpart, long-term depression (LTD). Hebbian forms of plasticity typically function in an input-specific manner, are rapidly induced and long-lasting, and require correlated firing of the pre-and post-synaptic neurons (Malenka and Bear 2004;Luscher and Malenka 2012;Huganir and Nicoll 2013). Because these hallmark features facilitate the reinforcement of precise synaptic connections, which is fundamental for information storage in the brain, these Hebbian mechanisms are thought to be the cellular correlates of learning and memory. However, these same features of Hebbian plasticity pose a stability problem to neural networks. The requirement of correlated activity to reinforce useful pathways in the brain provokes positive feedback loops of activity-dependent changes in synaptic strength. For instance, once LTP is induced, potentiated synapses are more excitable and can undergo further potentiation more easily, entering a cycle that, if unconstrained, eventually drives activity to a state prone to hyperexcitability

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“…The interaction of the different modalities can be uncovered during the loss of a sensory modality, which often leads to enhanced function of one or more of the remaining senses in a process often termed “cross-modal plasticity” (Bavelier and Neville, 2002; Lee and Whitt, 2015). The best-studied group of individuals are the early or late blind, who can show enhanced performance in the remaining senses, for example better sound localization (Lessard et al, 1998; Röder et al, 1999) and pitch discrimination (Gougoux et al, 2004), than sighted individuals.…”

Section: Introductionmentioning

confidence: 99%