Burst detection algorithms for the analysis of spatio-temporal patterns in cortical networks of neurons

Chiappalone, Michela; Novellino, Antonio; Vajda, Ildikó; Vato, Alessandro; Martinoia, Sergio; Pelt, Jaap van

doi:10.1016/j.neucom.2004.10.094

Cited by 134 publications

(131 citation statements)

References 14 publications

Supporting

Mentioning

129

Contrasting

Order By: Relevance

“…All further analyses on the spike trains were computed by custom scripts in Python. In particular, bursting activity was detected with a single channel spike train burst detector (46) and network-wide activity was characterized by MFR, MBR, and MBD, computed only on active channels (i.e., firing rate > 0.1 Hz). Functional connectivity analysis was performed by crosscorrelating spike events among electrodes, and the strongest (i.e., most correlated) 100 to 200 links were considered.…”

Section: High-density Meamentioning

confidence: 99%

Dominant β-catenin mutations cause intellectual disability with recognizable syndromic features

Tucci¹,

Kleefstra²,

Hardy³

et al. 2014

J. Clin. Invest.

116

128

View full text Add to dashboard Cite

The recent identification of multiple dominant mutations in the gene encoding β-catenin in both humans and mice has enabled exploration of the molecular and cellular basis of β-catenin function in cognitive impairment. In humans, β-catenin mutations that cause a spectrum of neurodevelopmental disorders have been identified. We identified de novo β-catenin mutations in patients with intellectual disability, carefully characterized their phenotypes, and were able to define a recognizable intellectual disability syndrome. In parallel, characterization of a chemically mutagenized mouse line that displays features similar to those of human patients with β-catenin mutations enabled us to investigate the consequences of β-catenin dysfunction through development and into adulthood. The mouse mutant, designated batface (Bfc), carries a Thr653Lys substitution in the C-terminal armadillo repeat of β-catenin and displayed a reduced affinity for membrane-associated cadherins. In association with this decreased cadherin interaction, we found that the mutation results in decreased intrahemispheric connections, with deficits in dendritic branching, long-term potentiation, and cognitive function. Our study provides in vivo evidence that dominant mutations in β-catenin underlie losses in its adhesion-related functions, which leads to severe consequences, including intellectual disability, childhood hypotonia, progressive spasticity of lower limbs, and abnormal craniofacial features in adults. Introduction β-Catenin (CTNNB1) is a highly conserved protein that implements key cellular functions by interacting with cell-adhesion proteins, signaling molecules, and transcription factors (1). The characteristic structural feature of the β-catenin protein, its 12 central armadillo repeats, forms a long positively charged groove facilitating interaction with multiple protein partners. This central motif is flanked by the N terminus, crucial in mediating degradation of the protein, and the C terminus, containing the Helix-C motif (2), which enables switching between the protein's dual roles in cell adhesion and proliferation. Loss-of-function studies in mammals have implicated β-catenin in embryonic development, while gain-of-function studies have demonstrated its contribution to various forms of human cancers (reviewed in ref.3). Functional investigation has focused on the role of β-catenin in canonical WNT signaling. β-Catenin interacts with transcriptional coactivators to mediate WNT's transcriptional activation, which orchestrates growth and patterning in the developing embryo, and, when constitutively upregulated, dysregulates growth connected to cancer and metastasis.

show abstract

Section: High-density Meamentioning

confidence: 99%

Dominant β-catenin mutations cause intellectual disability with recognizable syndromic features

Tucci¹,

Kleefstra²,

Hardy³

et al. 2014

J. Clin. Invest.

116

128

View full text Add to dashboard Cite

show abstract

“…The BD algorithm we are presenting is based on previously developed methods (Chiappalone et al 2005;Turnbull et al 2005). According to those algorithms, in order to detect bursts, two thresholds were fixed: the first one was the maximum ISI allowed for spikes within a burst (maxISI, usually set at 100 ms); the second one was defined as the minimum number of consecutive spikes belonging to a burst (minSpikes, usually set at 5).…”

Section: Bd Algorithmmentioning

confidence: 99%

“…Several methods have been proposed in the literature for burst detection and analysis of in vivo and/or in vitro recordings (Chiappalone et al 2005;Gourevitch and Eggermont 2007;Ham et al 2008;Legendy and Salcman 1985;Selinger et al 2007;Turnbull et al 2005;Wagenaar et al 2005a). In our work we decided to focus mainly on the algorithms proposed for the in vitro recordings.…”

mentioning

confidence: 99%

“…Starting from the method we proposed a few years ago (Chiappalone et al 2005), we developed a new and more reliable burst detection (BD) algorithm based on the evaluation of the logarithmic inter-spike interval histogram (logISIH) in order to look for the best threshold between intra-burst (i.e. within bursts) and inter-burst (i.e.…”

mentioning

confidence: 99%

“…trains containing only the first spike of each burst) to detect the network bursts (network burst detection, NBD), following a procedure similar to that used for the detection of single-channel bursts. We tested the new algorithms on a sample data set and compared them with a series of methods already presented in the literature (Chiappalone et al 2005;Gourevitch and Eggermont 2007;Selinger et al 2007;van Pelt et al 2004;Wagenaar et al 2005a).…”

mentioning

confidence: 99%

See 2 more Smart Citations

A self-adapting approach for the detection of bursts and network bursts in neuronal cultures

2009

View full text Add to dashboard Cite

Dissociated networks of neurons typically exhibit bursting behavior, whose features are strongly influenced by the age of the culture, by chemical/electrical stimulation or by environmental conditions. To help the experimenter in identifying the changes possibly induced by specific protocols, we developed a self-adapting method for detecting both bursts and network bursts from electrophysiological activity recorded by means of micro-electrode arrays. The algorithm is based on the computation of the logarithmic inter-spike interval histogram and automatically detects the best threshold to distinguish between inter- and intra-burst inter-spike intervals for each recording channel of the array. An analogous procedure is followed for the detection of network bursts, looking for sequences of closely spaced single-channel bursts. We tested our algorithm on recordings of spontaneous as well as chemically stimulated activity, comparing its performance to other methods available in the literature.

show abstract

HDAC6 Inhibition Corrects Electrophysiological and Axonal Transport Deficits in a Human Stem Cell‐Based Model of Charcot‐Marie‐Tooth Disease (Type 2D)

et al. 2021

View full text Add to dashboard Cite

Charcot‐Marie‐Tooth disease type 2D (CMT2D), is a hereditary peripheral neuropathy caused by mutations in the gene encoding glycyl‐tRNA synthetase (GARS1). Here, human induced pluripotent stem cell (hiPSC)‐based models of CMT2D bearing mutations in GARS1 and their use for the identification of predictive biomarkers amenable to therapeutic efficacy screening is described. Cultures containing spinal cord motor neurons generated from this line exhibit network activity marked by significant deficiencies in spontaneous action potential firing and burst fire behavior. This result matches clinical data collected from a patient bearing a GARS1P724H mutation and is coupled with significant decreases in acetylated α‐tubulin levels and mitochondrial movement within axons. Treatment with histone deacetylase 6 inhibitors, tubastatin A and CKD504, improves mitochondrial movement and α‐tubulin acetylation in these cells. Furthermore, CKD504 treatment enhances population‐level electrophysiological activity, highlighting its potential as an effective treatment for CMT2D.

show abstract

Burst detection algorithms for the analysis of spatio-temporal patterns in cortical networks of neurons

Cited by 134 publications

References 14 publications

Dominant β-catenin mutations cause intellectual disability with recognizable syndromic features

Dominant β-catenin mutations cause intellectual disability with recognizable syndromic features

A self-adapting approach for the detection of bursts and network bursts in neuronal cultures

HDAC6 Inhibition Corrects Electrophysiological and Axonal Transport Deficits in a Human Stem Cell‐Based Model of Charcot‐Marie‐Tooth Disease (Type 2D)

Contact Info

Product

Resources

About