Decrease in Calcium Concentration Triggers Neuronal Retinoic Acid Synthesis during Homeostatic Synaptic Plasticity

Wang, Huili; Zhang, Zhenjie; Hintze, Maik; Chen, Lu

doi:10.1523/jneurosci.3964-11.2011

Cited by 95 publications

(136 citation statements)

References 30 publications

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“…In contrast to our study, other studies have shown that atRA often induces increases in Ca 2ϩ levels, either directly through release from intracellular stores (Liou et al 2005), or indirectly as a result of increased AMPA receptor function (Wang et al 2011). However, these previous studies examined either developing synapses or those undergoing activity-induced plasticity.…”

Section: Discussioncontrasting

confidence: 99%

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Retinoic acid affects calcium signaling in adult molluscan neurons

Vesprini

Dawson

Yuan

et al. 2015

Journal of Neurophysiology

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acid, the active metabolite of vitamin A, is important for nervous system development, regeneration, as well as cognitive functions of the adult central nervous system. These central nervous system functions are all highly dependent on neuronal activity. Retinoic acid has previously been shown to induce changes in the firing properties and action potential waveforms of adult molluscan neurons in a dose-and isomer-dependent manner. In this study, we aimed to determine the cellular pathways by which retinoic acid might exert such effects, by testing the involvement of pathways previously shown to be affected by retinoic acid. We demonstrated that the ability of all-trans retinoic acid (atRA) to induce electrophysiological changes in cultured molluscan neurons was not prevented by inhibitors of protein synthesis, protein kinase A or phospholipase C. However, we showed that atRA was capable of rapidly reducing intracellular calcium levels in the same dose-and isomer-dependent manner as shown previously for changes in neuronal firing. Moreover, we also demonstrated that the transmembrane ion flux through voltage-gated calcium channels was rapidly modulated by retinoic acid. In particular, the peak current density was reduced and the inactivation rate was increased in the presence of atRA, over a similar time course as the changes in cell firing and reductions in intracellular calcium. These studies provide further evidence for the ability of atRA to induce rapid effects in mature neurons.

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Section: Discussioncontrasting

confidence: 99%

“…Micromolar concentrations of atRA regulate synaptic strength between neurons , and this role in homeostatic plasticity is regulated by postsynaptic Ca 2ϩ (Wang et al 2011). It was shown that reductions in postsynaptic Ca 2ϩ levels activated RA synthesis, and it was concluded that neuronal RA synthesis is tightly regulated by [Ca 2ϩ ] i .…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid affects calcium signaling in adult molluscan neurons

Vesprini

Dawson

Yuan

et al. 2015

Journal of Neurophysiology

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“…RA synthesis is triggered by reduced excitatory synaptic transmission and decreased dendritic calcium levels [128,129]. The RA receptor RARa is a classical DNA-binding nuclear receptor rstb.royalsocietypublishing.org Phil.…”

Section: (B) Distinct Players In Homeostatic Plasticitymentioning

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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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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“…Having established the connection between CaN activity and RA signaling, we next asked whether CaN is involved in activity blockade-induced homeostatic plasticity, which requires RA signaling (4,6). We performed three lines of experiments to test this.…”

Section: Ra Receptor Rarα Mediates Can Inhibitor-induced Regulation Ofmentioning

confidence: 99%

“…It also has been shown that dendritic Ca 2+ levels directly govern the synthesis of RA; basal Ca 2+ levels maintained by normal synaptic transmission are sufficient to suppress RA synthesis. Upon synaptic activity inhibition, reduced Ca 2+ levels de-repress RA synthesis and activate RA-dependent homeostatic synaptic mechanisms (6). Thus, a Ca 2+ -dependent signaling molecule that is sensitive to changes in basal Ca 2+ levels must be involved in synaptic RA signaling.…”

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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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Decrease in Calcium Concentration Triggers Neuronal Retinoic Acid Synthesis during Homeostatic Synaptic Plasticity

Cited by 95 publications

References 30 publications

Retinoic acid affects calcium signaling in adult molluscan neurons

Retinoic acid affects calcium signaling in adult molluscan neurons

A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

Calcineurin mediates homeostatic synaptic plasticity by regulating retinoic acid synthesis

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