Homeostatic Control of Presynaptic Neurotransmitter Release

Davis, Graeme W.; Müller, Martin

doi:10.1146/annurev-physiol-021014-071740

Cited by 243 publications

(275 citation statements)

References 112 publications

(183 reference statements)

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“…R. Soc. B 372: 20160155 reviews [17,19,20,72,73]. Instead, we focus on the molecular intersection and distinctions between Hebbian and homeostatic synaptic plasticity at central mammalian synapses.…”

Section: Cellular and Molecular Mechanisms: Overlapping And Distinct mentioning

confidence: 99%

“…It is now clear that network activity is a key parameter for the physiology of the nervous system, and that homeostatic mechanisms that maintain the stability of a network must exist [15,16]. In the past two decades, neuroscientists have made significant progress towards characterization and mechanistic appreciation of homeostatic plasticity in both vertebrates and invertebrates [17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

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A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

Yee¹,

Hsu²,

Chen³

2017

Phil. Trans. R. Soc. B

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One contribution of 16 to a discussion meeting issue 'Integrating Hebbian and homeostatic plasticity'. Hebbian and homeostatic plasticity are two major forms of plasticity in the nervous system: Hebbian plasticity provides a synaptic basis for associative learning, whereas homeostatic plasticity serves to stabilize network activity. While achieving seemingly very different goals, these two types of plasticity interact functionally through overlapping elements in their respective mechanisms. Here, we review studies conducted in the mammalian central nervous system, summarize known circuit and molecular mechanisms of homeostatic plasticity, and compare these mechanisms with those that mediate Hebbian plasticity. We end with a discussion of 'local' homeostatic plasticity and the potential role of local homeostatic plasticity as a form of metaplasticity that modulates a neuron's future capacity for Hebbian plasticity.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.

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Section: Cellular and Molecular Mechanisms: Overlapping And Distinct mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

Yee¹,

Hsu²,

Chen³

2017

Phil. Trans. R. Soc. B

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“…Homeostatic plasticity of synapses has been shown in a variety of animal models to include changes in excitability, regulation of neurotransmitter release, or regulation of postsynaptic neurotransmitter receptors. The molecular pathways that contribute to homeostatic plasticity in Drosophila NMJ and other systems has been recently reviewed (Davis 2013;Davis and Müller 2014;Frank 2014). We will briefly discuss some key findings below.…”

Section: Homeostatic Plasticitymentioning

confidence: 99%

Transmission, Development, and Plasticity of Synapses

Harris¹,

2015

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Chemical synapses are sites of contact and information transfer between a neuron and its partner cell. Each synapse is a specialized junction, where the presynaptic cell assembles machinery for the release of neurotransmitter, and the postsynaptic cell assembles components to receive and integrate this signal. Synapses also exhibit plasticity, during which synaptic function and/or structure are modified in response to activity. With a robust panel of genetic, imaging, and electrophysiology approaches, and strong evolutionary conservation of molecular components, Drosophila has emerged as an essential model system for investigating the mechanisms underlying synaptic assembly, function, and plasticity. We will discuss techniques for studying synapses in Drosophila, with a focus on the larval neuromuscular junction (NMJ), a well-established model glutamatergic synapse. Vesicle fusion, which underlies synaptic release of neurotransmitters, has been well characterized at this synapse. In addition, studies of synaptic assembly and organization of active zones and postsynaptic densities have revealed pathways that coordinate those events across the synaptic cleft. We will also review modes of synaptic growth and plasticity at the fly NMJ, and discuss how pre-and postsynaptic cells communicate to regulate plasticity in response to activity. KEYWORDS FlyBook; Drosophila; synapse; neurotransmitter release; synaptic plasticity; active zone; synaptic vesicle TABLE OF CONTENTS Abstract 345Introduction 345

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“…Homeostatic synaptic plasticity is a type of compensatory mechanism activated during chronic elevation or reduction of network activity to modulate synaptic strength in the opposite direction (for example, reduced network activity leads to increased synaptic strength) (1,2). Retinoic acid (RA) is a key signaling molecule in a form of homeostatic synaptic plasticity induced by reduced excitatory synaptic activity (3)(4)(5).…”

mentioning

confidence: 99%

Calcineurin mediates homeostatic synaptic plasticity by regulating retinoic acid synthesis

Arendt

Zhang

Ganesan

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Homeostatic synaptic plasticity is a form of non-Hebbian plasticity that maintains stability of the network and fidelity for information processing in response to prolonged perturbation of network and synaptic activity. Prolonged blockade of synaptic activity decreases resting Ca2+ levels in neurons, thereby inducing retinoic acid (RA) synthesis and RA-dependent homeostatic synaptic plasticity; however, the signal transduction pathway that links reduced Ca2+-levels to RA synthesis remains unknown. Here we identify the Ca2+-dependent protein phosphatase calcineurin (CaN) as a key regulator for RA synthesis and homeostatic synaptic plasticity. Prolonged inhibition of CaN activity promotes RA synthesis in neurons, and leads to increased excitatory and decreased inhibitory synaptic transmission. These effects of CaN inhibitors on synaptic transmission are blocked by pharmacological inhibitors of RA synthesis or acute genetic deletion of the RA receptor RARα. Thus, CaN, acting upstream of RA, plays a critical role in gating RA signaling pathway in response to synaptic activity. Moreover, activity blockade-induced homeostatic synaptic plasticity is absent in CaN knockout neurons, demonstrating the essential role of CaN in RA-dependent homeostatic synaptic plasticity. Interestingly, in GluA1 S831A and S845A knockin mice, CaN inhibitor- and RA-induced regulation of synaptic transmission is intact, suggesting that phosphorylation of GluA1 C-terminal serine residues S831 and S845 is not required for CaN inhibitor- or RA-induced homeostatic synaptic plasticity. Thus, our study uncovers an unforeseen role of CaN in postsynaptic signaling, and defines CaN as the Ca2+-sensing signaling molecule that mediates RA-dependent homeostatic synaptic plasticity.

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Homeostatic Control of Presynaptic Neurotransmitter Release

Cited by 243 publications

References 112 publications

A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

Transmission, Development, and Plasticity of Synapses

Calcineurin mediates homeostatic synaptic plasticity by regulating retinoic acid synthesis

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