Search bioRxivSearch

bioRxiv · 10.1101/2020.12.22.424015

A Simple Method for Getting Standard Error on the Ratiometric Calcium Estimator

Abstract

1.The ratiometric fluorescent calcium indicator Fura-2 plays a fundamental role in the investigation of cellular calcium dynamics. Despite of its widespread use in the last 30 years, only one publication [2] proposed a way of obtaining confidence intervals on fitted calcium dynamic model parameters from single calcium transients. Shortcomings of this approach are its requirement for a 3 wavelengths protocol (excitation at 340 and 380 nm as usual plus at 360 nm, the isosbectic point) as well as the need for an autofluorence / background fluorescence model at each wavelength. We propose here a simpler method that eliminates both shortcommings: O_LIa precise estimation of the standard errors of the raw data is obtained first, C_LIO_LIthe standard error of the ratiometric calcium estimator (a function of the raw data values) is derived using both the propagation of uncertainty and a Monte-Carlo method. C_LI Once meaningful standard errors for calcium estimates are available, standard errors on fitted model parameters follow directly from the use of nonlinear least-squares optimization algorithms. 2. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=158 SRC="FIGDIR/small/424015v1_fig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@c830a6org.highwire.dtl.DTLVardef@f20cbforg.highwire.dtl.DTLVardef@122fb2aorg.highwire.dtl.DTLVardef@197b331_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 1:C_FLOATNO How to get error bars on the ratiometric calcium estimator? The figure is to be read clockwise from the bottom right corner. The two measurements areas (region of interest, ROI, on the cell body and background measurement region, BMR, outside of the cell) are displayed on the frame corresponding to one actual experiment. Two measurements, one following an excitation at 340 nm and the other following an excitation at 380 nm are performed (at each time point) from each region. The result is a set of four measures: adu340 (from the ROI), adu340B (from the BMR), adu380 and adu380B. These measurements are modeled as realizations of Gaussian random variables. The fact that the measurements as well as the subsequent quantities derived from them are random variable realization is conveyed throughout the figure by the use of Gaussian probability densities. The densities from the MRB are tighter because there are much more pixels in the MRB than in the ROI (the standard deviations of the densities shown on this figure have been enlarged for clarity, but their relative size has been preserved, the horizontal axis in black always starts at 0). The key result of the paper is that the standard deviation of the four Gaussian densities corresponding to the raw data (bottom of the figure) can be reliably estimated from the data alone, [Figure 1], where V is the product of the CCD chip gain squared by the number of pixels in the ROI by the CCD chip readout variance. The algebric operations leading to the estimator (top right) are explicitely displayed. The paper explains how to compute the standard deviation of the derived distributions obtained at each step of the calcium concentration estimation. C_FIG Method nameStandard error for the ratiometric calcium estimator

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hess, S., Pouzat, C., Kloppenburg, P.. 2020-12-23. A Simple Method for Getting Standard Error on the Ratiometric Calcium Estimator. https://doi.org/10.1101/2020.12.22.424015

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience