Faculty Opinions recommendation of MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity.

2018 ◽  
Author(s):  
Johannes Hell
Keyword(s):  
Synaptic Plasticity ◽  
Homeostatic Synaptic Plasticity

scholarly journals Homeostatic synaptic depression is achieved through a regulated decrease in presynaptic calcium channel abundance

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Michael A Gaviño ◽  
Kevin J Ford ◽  
Santiago Archila ◽  
Graeme W Davis
Keyword(s):  
Synaptic Plasticity ◽  
Neuromuscular Junction ◽  
Action Potential ◽  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Calcium Influx ◽  
Homeostatic Synaptic Plasticity ◽  
Action Potential Waveform ◽  
Presynaptic Calcium ◽  
Potential Waveform

Homeostatic signaling stabilizes synaptic transmission at the neuromuscular junction (NMJ) of Drosophila, mice, and human. It is believed that homeostatic signaling at the NMJ is bi-directional and considerable progress has been made identifying mechanisms underlying the homeostatic potentiation of neurotransmitter release. However, very little is understood mechanistically about the opposing process, homeostatic depression, and how bi-directional plasticity is achieved. Here, we show that homeostatic potentiation and depression can be simultaneously induced, demonstrating true bi-directional plasticity. Next, we show that mutations that block homeostatic potentiation do not alter homeostatic depression, demonstrating that these are genetically separable processes. Finally, we show that homeostatic depression is achieved by decreased presynaptic calcium channel abundance and calcium influx, changes that are independent of the presynaptic action potential waveform. Thus, we identify a novel mechanism of homeostatic synaptic plasticity and propose a model that can account for the observed bi-directional, homeostatic control of presynaptic neurotransmitter release.

scholarly journals Astrocyte-secreted IL-33 mediates homeostatic synaptic plasticity in the adult hippocampus

2020 ◽  
Vol 118 (1) ◽  
pp. e2020810118
Author(s):  
Ye Wang ◽  
Wing-Yu Fu ◽  
Kit Cheung ◽  
Kwok-Wang Hung ◽  
Congping Chen ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Activity ◽  
Hippocampal Slices ◽  
Memory Formation ◽  
Conditional Knockout ◽  
Acute Administration ◽  
Excitatory Synapses ◽  
Homeostatic Synaptic Plasticity ◽  
Hippocampal Ca1

Hippocampal synaptic plasticity is important for learning and memory formation. Homeostatic synaptic plasticity is a specific form of synaptic plasticity that is induced upon prolonged changes in neuronal activity to maintain network homeostasis. While astrocytes are important regulators of synaptic transmission and plasticity, it is largely unclear how they interact with neurons to regulate synaptic plasticity at the circuit level. Here, we show that neuronal activity blockade selectively increases the expression and secretion of IL-33 (interleukin-33) by astrocytes in the hippocampal cornu ammonis 1 (CA1) subregion. This IL-33 stimulates an increase in excitatory synapses and neurotransmission through the activation of neuronal IL-33 receptor complex and synaptic recruitment of the scaffold protein PSD-95. We found that acute administration of tetrodotoxin in hippocampal slices or inhibition of hippocampal CA1 excitatory neurons by optogenetic manipulation increases IL-33 expression in CA1 astrocytes. Furthermore, IL-33 administration in vivo promotes the formation of functional excitatory synapses in hippocampal CA1 neurons, whereas conditional knockout of IL-33 in CA1 astrocytes decreases the number of excitatory synapses therein. Importantly, blockade of IL-33 and its receptor signaling in vivo by intracerebroventricular administration of its decoy receptor inhibits homeostatic synaptic plasticity in CA1 pyramidal neurons and impairs spatial memory formation in mice. These results collectively reveal an important role of astrocytic IL-33 in mediating the negative-feedback signaling mechanism in homeostatic synaptic plasticity, providing insights into how astrocytes maintain hippocampal network homeostasis.

scholarly journals Synaptic Signaling by All-Trans Retinoic Acid in Homeostatic Synaptic Plasticity

Neuron ◽  
2008 ◽  
Vol 60 (2) ◽  
pp. 308-320 ◽  
Author(s):  
Jason Aoto ◽  
Christine I. Nam ◽  
Michael M. Poon ◽  
Pamela Ting ◽  
Lu Chen
Keyword(s):  
Retinoic Acid ◽  
Synaptic Plasticity ◽  
Synaptic Signaling ◽  
Homeostatic Synaptic Plasticity ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

scholarly journals What goes up must come down: homeostatic synaptic plasticity strategies in neurological disease

2018 ◽  
Vol 13 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Emily A André ◽  
Patrick A Forcelli ◽  
Daniel TS Pak
Keyword(s):  
Synaptic Plasticity ◽  
Neurological Disease ◽  
Homeostatic Synaptic Plasticity

scholarly journals Role of neuronal activity and metaplastic state in homeostatic synaptic plasticity

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S402-S403
Author(s):  
Bryce Grier ◽  
Varun Chokshi ◽  
Andrew Dykman ◽  
Crystal Lantz ◽  
Ernst Niebur ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Activity ◽  
Homeostatic Synaptic Plasticity

scholarly journals Phosphorylation of AMPA Receptors Is Required for Sensory Deprivation-Induced Homeostatic Synaptic Plasticity

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e18264 ◽  
Author(s):  
Anubhuti Goel ◽  
Linda W. Xu ◽  
Kevin P. Snyder ◽  
Lihua Song ◽  
Yamila Goenaga-Vazquez ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Ampa Receptors ◽  
Sensory Deprivation ◽  
Homeostatic Synaptic Plasticity

scholarly journals Modulation of network activity and induction of homeostatic synaptic plasticity by enzymatic removal of heparan sulfates

2014 ◽  
Vol 369 (1654) ◽  
pp. 20140134 ◽  
Author(s):  
Svetlana Korotchenko ◽  
Lorenzo A. Cingolani ◽  
Tatiana Kuznetsova ◽  
Luca Leonardo Bologna ◽  
Michela Chiappalone ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Network Activity ◽  
Strong Increase ◽  
Bioelectrical Activity ◽  
Highly Active ◽  
Homeostatic Synaptic Plasticity ◽  
Term Potentiation ◽  
Heparan Sulfates

Heparan sulfates (HSs) are complex and highly active molecules that are required for synaptogenesis and long-term potentiation. A deficit in HSs leads to autistic phenotype in mice. Here, we investigated the long-term effect of heparinase I, which digests highly sulfated HSs, on the spontaneous bioelectrical activity of neuronal networks in developing primary hippocampal cultures. We found that chronic heparinase treatment led to a significant reduction of the mean firing rate of neurons, particularly during the period of maximal neuronal activity. Furthermore, firing pattern in heparinase-treated cultures often appeared as epileptiform bursts, with long periods of inactivity between them. These changes in network activity were accompanied by an increase in the frequency and amplitude of miniature postsynaptic excitatory currents, which could be described by a linear up-scaling of current amplitudes. Biochemically, we observed an upregulation in the expression of the glutamate receptor subunit GluA1, but not GluA2, and a strong increase in autophosphorylation of α and β Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), without changes in the levels of kinase expression. These data suggest that a deficit in HSs triggers homeostatic synaptic plasticity and drastically affects functional maturation of neural network.

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