Use of multi-electrode array recordings in studies of network synaptic plasticity in both time and space

Liu, Ming-Gang; Chen, Xuefeng; He, Ting; Li, Zhen

doi:10.1007/s12264-012-1251-5

Cited by 41 publications

(30 citation statements)

References 49 publications

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“…In in-vitro networks, multielectrode arrays (MEAs) can be used to stimulate many neurons at the same time, as well as to measure their activity [46]. For our purposes, an MEA could be used to trigger plasticity, forming a strongly interconnected cell assembly.…”

Section: Testing Our Predictions In Experimentsmentioning

confidence: 99%

Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

Luboeinski

Tetzlaff

2020

Preprint

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The synaptic-tagging-and-capture (STC) hypothesis formulates that at each synapse the concurrence of a tag with protein synthesis yields the maintenance of changes induced by synaptic plasticity. This hypothesis provides a biological principle underlying the synaptic consolidation of memories that is not verified for recurrent neural circuits. We developed a theoretical model integrating the mechanisms underlying the STC hypothesis with calcium-based synaptic plasticity in a recurrent spiking neural network. In the model, calcium-based synaptic plasticity yields the formation of strongly interconnected cell assemblies encoding memories, followed by consolidation through the STC mechanisms. Furthermore, we find that the STC mechanisms have an up to now undiscovered effect on memorieswith the passage of time they modify the storage of memories, such that after several hours memory recall is significantly improved. This kind of memory enhancement can provide a new principle for storing information in biological and artificial neural circuits.

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Section: Testing Our Predictions In Experimentsmentioning

confidence: 99%

Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

Luboeinski

Tetzlaff

2020

Preprint

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“…In the field of modern in vitro neuroscience, a mainstay methodology to study network-level electrophysiological properties of neuronal cell ensembles relies on non invasive substrateintegrated matrices of microelectrodes (i.e., Microelectrode Arrays or MEAs) functioning as interfaces between neuronal cultures and electronic readout systems (Johnstone et al, 2010;Nam and Wheeler, 2011;Obien et al, 2015). Nowadays, MEAs are routinely deployed in a bulk of applications, spanning studies about network dynamics (Biffi et al, 2013;Li et al, 2007;Wagenaar et al, 2006), neuronal plasticity (Liu et al, 2012), and drug screenings (Johnstone et al, 2010;Robinette et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Development of a bench‐top device for parallel climate‐controlled recordings of neuronal cultures activity with microelectrode arrays

Regalia

Biffi

Achilli

et al. 2015

Biotech & Bioengineering

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Two binding requirements for in vitro studies on long-term neuronal networks dynamics are (i) finely controlled environmental conditions to keep neuronal cultures viable and provide reliable data for more than a few hours and (ii) parallel operation on multiple neuronal cultures to shorten experimental time scales and enhance data reproducibility. In order to fulfill these needs with a Microelectrode Arrays (MEA)-based system, we designed a stand-alone device that permits to uninterruptedly monitor neuronal cultures activity over long periods, overcoming drawbacks of existing MEA platforms. We integrated in a single device: (i) a closed chamber housing four MEAs equipped with access for chemical manipulations, (ii) environmental control systems and embedded sensors to reproduce and remotely monitor the standard in vitro culture environment on the lab bench (i.e. in terms of temperature, air CO2 and relative humidity), and (iii) a modular MEA interface analog front-end for reliable and parallel recordings. The system has been proven to assure environmental conditions stable, physiological and homogeneos across different cultures. Prolonged recordings (up to 10 days) of spontaneous and pharmacologically stimulated neuronal culture activity have not shown signs of rundown thanks to the environmental stability and have not required to withdraw the cells from the chamber for culture medium manipulations. This system represents an effective MEA-based solution to elucidate neuronal network phenomena with slow dynamics, such as long-term plasticity, effects of chronic pharmacological stimulations or late-onset pathological mechanisms.

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“…However, this is consistent with many other studies in mouse models of DS and GEFS+ that show unaltered excitability of pyramidal neurons (Cheah et The ultimate goal of our study is to develop mechanism-based drug therapies using our mouse model that recapitulates seizure phenotypes in human patients. The micro-electrode array (MEA) system is emerging as a powerful tool to examine long term neural network activity in rodent brain slices or neuronal cultures in response to pharmacological drugs (Jensen, 2019;Liu et al, 2012;McConnell et al, 2012;Valdivia et al, 2014). Previous studies have shown that the MEA can be utilized for recording spontaneous neuronal activity from acute hippocampal cultures derived from R1648H mouse (Hedrich et al, 2014) and screen anti-convulsant drugs in rat brain slices (Fan et al, 2019).…”

Section: Comparison With the Existing Models Of K1270t Mutationmentioning

confidence: 99%

Interneuron dysfunction in a new knock-in mouse model of SCN1A GEFS+

Zhu

Xie

et al. 2019

Preprint

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Advances in genome sequencing have identified over 1300 mutations in the SCN1A sodium channel gene that result in genetic epilepsies. However, how individual mutations within SCN1A produce seizures remains elusive for most mutations. Previous work from our lab has shown that the K1270T (KT) mutation, which is linked to GEFS+ (Genetic Epilepsy with Febrile Seizure plus) in humans, causes reduced firing of GABAergic neurons in a Drosophila knock-in model. To examine the effect of this mutation in mammals, we introduced the equivalent KT mutation into the mouse Scn1a (Scn1a KT ) gene using CRISPR/Cas9. Mouse lines carrying this mutation were examined in two widely used genetic backgrounds, C57BL/6NJ and 129X1/SvJ. In both backgrounds, homozygous mutants had spontaneous seizures and died by postnatal day 23. There was no difference in the lifespan of mice heterozygous for the mutation in either background when compared to wild-type littermates up to 6 months. Heterozygous mutants had heat-induced seizures at ~42 deg. Celsius, a temperature that did not induce seizures in wild-type littermates. In acute hippocampal slices, current-clamp recordings revealed a significant depolarized shift in action potential threshold and reduced action potential amplitude in parvalbumin-expressing inhibitory interneurons in Scn1a KT/+ mice. There was no change in the firing properties of excitatory CA1 pyramidal neurons. Our results indicate that Scn1a KT/+ mice develop seizures, and impaired action potential firing of inhibitory interneurons in Scn1a KT/+ mice may produce hyperexcitability in the hippocampus.

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Use of multi-electrode array recordings in studies of network synaptic plasticity in both time and space

Cited by 41 publications

References 49 publications

Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

Development of a bench‐top device for parallel climate‐controlled recordings of neuronal cultures activity with microelectrode arrays

Interneuron dysfunction in a new knock-in mouse model of SCN1A GEFS+

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