scholarly journals CA 10 and CA 11 negatively regulate neuronal activity‐dependent growth of gliomas

2019 ◽  
Vol 13 (5) ◽  
pp. 1018-1032
Author(s):  
Bangbao Tao ◽  
Yiqun Ling ◽  
Youyou Zhang ◽  
Shu Li ◽  
Ping Zhou ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Dependent Growth ◽  
Activity Dependent

scholarly journals Growth Rules for the Repair of Asynchronous Irregular Neuronal Networks after Peripheral Lesions

2019 ◽  
Author(s):  
Ankur Sinha ◽  
Christoph Metzner ◽  
Neil Davey ◽  
Roderick Adams ◽  
Michael Schmuker ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Network Model ◽  
Neuronal Networks ◽  
Structural Plasticity ◽  
Activity Levels ◽  
Peripheral Lesion ◽  
Simulation Results ◽  
Dependent Growth ◽  
Activity Dependent ◽  
The Brain

AbstractSeveral homeostatic mechanisms enable the brain to maintain desired levels of neuronal activity. One of these, homeostatic structural plasticity, has been reported to restore activity in networks disrupted by peripheral lesions by altering their neuronal connectivity. While multiple lesion experiments have studied the changes in neurite morphology that underlie modifications of synapses in these networks, the underlying mechanisms that drive these changes are yet to be explained. Evidence suggests that neuronal activity modulates neurite morphology and may stimulate neurites to selective sprout or retract to restore network activity levels. We developed a new spiking network model, simulations of which accurately reproduce network rewiring after peripheral lesions as reported in experiments, to study these activity dependent growth regimes of neurites. To ensure that our simulations closely resemble the behaviour of networks in the brain, we deafferent a biologically realistic network model that exhibits low frequency Asynchronous Irregular (AI) activity as observed in cerebral cortex.Our simulation results indicate that the re-establishment of activity in neurons both within and outside the deprived region, the Lesion Projection Zone (LPZ), requires opposite activity dependent growth rules for excitatory and inhibitory post-synaptic elements. Analysis of these growth regimes indicates that they also contribute to the maintenance of activity levels in individual neurons. Furthermore, in our model, the directional formation of synapses that is observed in experiments requires that pre-synaptic excitatory and inhibitory elements also follow opposite growth rules. Lastly, we observe that our proposed model of homeostatic structural plasticity and the inhibitory synaptic plasticity mechanism that also balances our AI network are both necessary for successful rewiring of the network.Author summaryAn accumulating body of evidence suggests that our brain can compensate for peripheral lesions by adaptive rewiring of its neuronal circuitry. The underlying process, structural plasticity, can modify the connectivity of neuronal networks in the brain, thus affecting their function. To better understand the mechanisms of structural plasticity in the brain, we have developed a novel model of peripheral lesions and the resulting activity-dependent rewiring in a simplified cortical network model that exhibits biologically realistic asynchronous irregular activity. In order to accurately reproduce the directionality and time course of rewiring after injury that is observed in peripheral lesion experiments, we derive activity dependent growth rules for different synaptic elements: dendritic and axonal contacts. Our simulation results suggest that excitatory and inhibitory synaptic elements have to react to changes in neuronal activity in opposite ways. We show that these rules result in a homeostatic stabilisation of activity in individual neurons. In our simulations, both synaptic and structural plasticity mechanisms are necessary for network repair. Furthermore, our simulations indicate that while activity is restored in neurons deprived by the peripheral lesion, the temporal firing characteristics of the network can be changed by the rewiring process.

scholarly journals Growth rules for the repair of Asynchronous Irregular neuronal networks after peripheral lesions

2021 ◽  
Vol 17 (6) ◽  
pp. e1008996
Author(s):  
Ankur Sinha ◽  
Christoph Metzner ◽  
Neil Davey ◽  
Roderick Adams ◽  
Michael Schmuker ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Network Model ◽  
Low Frequency ◽  
Structural Plasticity ◽  
Network Activity ◽  
Activity Levels ◽  
Dependent Growth ◽  
Underlying Mechanisms ◽  
Activity Dependent ◽  
The Brain

Several homeostatic mechanisms enable the brain to maintain desired levels of neuronal activity. One of these, homeostatic structural plasticity, has been reported to restore activity in networks disrupted by peripheral lesions by altering their neuronal connectivity. While multiple lesion experiments have studied the changes in neurite morphology that underlie modifications of synapses in these networks, the underlying mechanisms that drive these changes are yet to be explained. Evidence suggests that neuronal activity modulates neurite morphology and may stimulate neurites to selective sprout or retract to restore network activity levels. We developed a new spiking network model of peripheral lesioning and accurately reproduced the characteristics of network repair after deafferentation that are reported in experiments to study the activity dependent growth regimes of neurites. To ensure that our simulations closely resemble the behaviour of networks in the brain, we model deafferentation in a biologically realistic balanced network model that exhibits low frequency Asynchronous Irregular (AI) activity as observed in cerebral cortex. Our simulation results indicate that the re-establishment of activity in neurons both within and outside the deprived region, the Lesion Projection Zone (LPZ), requires opposite activity dependent growth rules for excitatory and inhibitory post-synaptic elements. Analysis of these growth regimes indicates that they also contribute to the maintenance of activity levels in individual neurons. Furthermore, in our model, the directional formation of synapses that is observed in experiments requires that pre-synaptic excitatory and inhibitory elements also follow opposite growth rules. Lastly, we observe that our proposed structural plasticity growth rules and the inhibitory synaptic plasticity mechanism that also balances our AI network both contribute to the restoration of the network to pre-deafferentation stable activity levels.

Extracellular Release of ILEI/FAM3C and Amyloid-β Is Associated with the Activation of Distinct Synapse Subpopulations

2021 ◽  
pp. 1-16
Author(s):  
Masaki Nakano ◽  
Yachiyo Mitsuishi ◽  
Lei Liu ◽  
Naoki Watanabe ◽  
Emi Hibino ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Epithelial Mesenchymal Transition ◽  
Surrogate Marker ◽  
Amyloid Β ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Extracellular Release ◽  
Activity Dependent ◽  
Aβ Production

Background: Brain amyloid-β (Aβ) peptide is released into the interstitial fluid (ISF) in a neuronal activity-dependent manner, and Aβ deposition in Alzheimer’s disease (AD) is linked to baseline neuronal activity. Although the intrinsic mechanism for Aβ generation remains to be elucidated, interleukin-like epithelial-mesenchymal transition inducer (ILEI) is a candidate for an endogenous Aβ suppressor. Objective: This study aimed to access the mechanism underlying ILEI secretion and its effect on Aβ production in the brain. Methods: ILEI and Aβ levels in the cerebral cortex were monitored using a newly developed ILEI-specific ELISA and in vivo microdialysis in mutant human Aβ precursor protein-knockin mice. ILEI levels in autopsied brains and cerebrospinal fluid (CSF) were measured using ELISA. Results: Extracellular release of ILEI and Aβ was dependent on neuronal activation and specifically on tetanus toxin-sensitive exocytosis of synaptic vesicles. However, simultaneous monitoring of extracellular ILEI and Aβ revealed that a spontaneous fluctuation of ILEI levels appeared to inversely mirror that of Aβ levels. Selective activation and inhibition of synaptic receptors differentially altered these levels. The evoked activation of AMPA-type receptors resulted in opposing changes to ILEI and Aβ levels. Brain ILEI levels were selectively decreased in AD. CSF ILEI concentration correlated with that of Aβ and were reduced in AD and mild cognitive impairment. Conclusion: ILEI and Aβ are released from distinct subpopulations of synaptic terminals in an activity-dependent manner, and ILEI negatively regulates Aβ production in specific synapse types. CSF ILEI might represent a surrogate marker for the accumulation of brain Aβ.

A Computational Study on Synaptic Plasticity Regulation and Information Processing in Neuron-Astrocyte Networks

2021 ◽  
pp. 1-23
Author(s):  
Roman Vuillaume ◽  
Jhunlyn Lorenzo ◽  
Stéphane Binczak ◽  
Sabir Jacquir
Keyword(s):  
Transfer Function ◽  
Neuronal Activity ◽  
Information Transfer ◽  
Computational Study ◽  
Regulation Of Expression ◽  
Ionotropic Receptors ◽  
Postsynaptic Activity ◽  
Outward Currents ◽  
Layered Networks ◽  
Activity Dependent

Abstract Postsynaptic ionotropic receptors critically shape synaptic currents and underpin their activity-dependent plasticity. In recent years, regulation of expression of these receptors by slow inward and outward currents mediated by gliotransmitter release from astrocytes has come under scrutiny as a potentially important mechanism for the regulation of synaptic information transfer. In this study, we consider a model of astrocyte-regulated synapses to investigate this hypothesis at the level of layered networks of interacting neurons and astrocytes. Our simulations hint that gliotransmission sustains the transfer function across layers, although it decorrelates the neuronal activity from the signal pattern. Overall, our results make clear how astrocytes could transform neuronal activity by inducing a lowfrequency modulation of postsynaptic activity.

scholarly journals Global sleep homeostasis reflects temporally and spatially integrated local cortical neuronal activity

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Christopher W Thomas ◽  
Mathilde CC Guillaumin ◽  
Laura E McKillop ◽  
Peter Achermann ◽  
Vladyslav V Vyazovskiy
Keyword(s):  
Neuronal Activity ◽  
Wave Activity ◽  
Neuronal Firing ◽  
Daily Amount ◽  
Local Process ◽  
Sleep Homeostasis ◽  
Freely Behaving ◽  
Electroencephalogram Eeg ◽  
Activity Dependent ◽  
Wake State

Sleep homeostasis manifests as a relative constancy of its daily amount and intensity. Theoretical descriptions define ‘Process S’, a variable with dynamics dependent on global sleep-wake history, and reflected in electroencephalogram (EEG) slow wave activity (SWA, 0.5–4 Hz) during sleep. The notion of sleep as a local, activity-dependent process suggests that activity history must be integrated to determine the dynamics of global Process S. Here, we developed novel mathematical models of Process S based on cortical activity recorded in freely behaving mice, describing local Process S as a function of the deviation of neuronal firing rates from a locally defined set-point, independent of global sleep-wake state. Averaging locally derived Processes S and their rate parameters yielded values resembling those obtained from EEG SWA and global vigilance states. We conclude that local Process S dynamics reflects neuronal activity integrated over time, and global Process S reflects local processes integrated over space.

An integrated microfluidic/microelectrode array for the study of activity-dependent intracellular dynamics in neuronal networks

Lab on a Chip ◽  
2018 ◽  
Vol 18 (22) ◽  
pp. 3425-3435 ◽  
Author(s):  
Eve Moutaux ◽  
Benoit Charlot ◽  
Aurélie Genoux ◽  
Frédéric Saudou ◽  
Maxime Cazorla
Keyword(s):  
Neuronal Activity ◽  
Neuronal Networks ◽  
Microelectrode Array ◽  
Activity Dependent

A microfluidics/MEA platform was developed to control neuronal activity while imaging intracellular dynamics within reconstituted neuronal networks.

scholarly journals Neurons and neuronal activity control gene expression in astrocytes to regulate their development and metabolism

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Philip Hasel ◽  
Owen Dando ◽  
Zoeb Jiwaji ◽  
Paul Baxter ◽  
Alison C. Todd ◽  
...  
Keyword(s):  
Gene Expression ◽  
Neuronal Activity ◽  
Cortical Neurons ◽  
Synaptic Activity ◽  
Rna Seq ◽  
Metabolic Cooperation ◽  
Closely Related Species ◽  
Lactate Shuttle ◽  
Activity Dependent ◽  
Elevated Lactate

Abstract The influence that neurons exert on astrocytic function is poorly understood. To investigate this, we first developed a system combining cortical neurons and astrocytes from closely related species, followed by RNA-seq and in silico species separation. This approach uncovers a wide programme of neuron-induced astrocytic gene expression, involving Notch signalling, which drives and maintains astrocytic maturity and neurotransmitter uptake function, is conserved in human development, and is disrupted by neurodegeneration. Separately, hundreds of astrocytic genes are acutely regulated by synaptic activity via mechanisms involving cAMP/PKA-dependent CREB activation. This includes the coordinated activity-dependent upregulation of major astrocytic components of the astrocyte–neuron lactate shuttle, leading to a CREB-dependent increase in astrocytic glucose metabolism and elevated lactate export. Moreover, the groups of astrocytic genes induced by neurons or neuronal activity both show age-dependent decline in humans. Thus, neurons and neuronal activity regulate the astrocytic transcriptome with the potential to shape astrocyte–neuron metabolic cooperation.

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