Search bioRxiv⌕ Search

Biology subjects

Bouchard, K.

Publications and source records attributed to Bouchard, K..

7 recordsLinked to original sources

A Generalist Intracortical Motor Decoder

Mapping the relationship between neural activity and motor behavior is a central aim of sensori-motor neuroscience and neurotechnology. While most progress to this end has relied on restricting complexity, the advent of foundation models instead proposes integrating a breadth of data as an alternate avenue for broadly advancing downstream modeling. We quantify this premise for motor decoding from intracortical microelectrode data, pretraining an autoregressive Transformer on 2000 hours of neural population spiking activity paired with diverse motor covariates from over 30 monkeys and humans. The resulting model is broadly useful, benefiting decoding on 8 downstream decoding tasks and generalizing to a variety of neural distribution shifts. However, we also highlight that scaling autoregressive Transformers seems unlikely to resolve limitations stemming from sensor variability and output stereotypy in neural datasets. Code: https://github.com/joel99/ndt3

neuroscience↗

Resolving Non-identifiability Mitigates Bias in Models of Neural Tuning and Functional Coupling

In the brain, all neurons are driven by the activity of other neurons, some of which maybe simultaneously recorded, but most are not. As such, models of neuronal activity need to account for simultaneously recorded neurons and the influences of unmeasured neurons. This can be done through inclusion of model terms for observed external variables (e.g., tuning to stimuli) as well as terms for latent sources of variability. Determining the influence of groups of neurons on each other relative to other influences is important to understand brain functioning. The parameters of statistical models fit to data are commonly used to gain insight into the relative importance of those influences. Scientific interpretation of models hinge upon unbiased parameter estimates. However, evaluation of biased inference is rarely performed and sources of bias are poorly understood. Through extensive numerical study and analytic calculation, we show that common inference procedures and models are typically biased. We demonstrate that accurate parameter selection before estimation resolves model non-identifiability and mitigates bias. In diverse neurophysiology data sets, we found that contributions of coupling to other neurons are often overestimated while tuning to exogenous variables are underestimated in common methods. We explain heterogeneity in observed biases across data sets in terms of data statistics. Finally, counter to common intuition, we found that model non-identifiability contributes to bias, not variance, making it a particularly insidious form of statistical error. Together, our results identify the causes of statistical biases in common models of neural data, provide inference procedures to mitigate that bias, and reveal and explain the impact of those biases in diverse neural data sets. 1 Author SummaryExperimental data of interacting cells under the influence of external as well as unobserved factors are ubiquitous. Parametric models are often used to gain understanding of the processes that generated such data. As such, biological understanding hinges upon accurate inference of model parameters. Whether and how systemic parameter bias manifests in such models is poorly understood. We study this issue in the specific context of estimating the static and dynamic interactions of simultaneously recorded neurons influenced by stimuli and unobserved neurons. Through extensive numerical study and analytic calculations, we identify and mitigate bias in such models. When applied to diverse neural data sets, we found that common models and inference procedures often overestimate the importance of coupling and underestimate tuning. In contrast to common intuition, we find that model non-identifiability contributes to estimation bias, not variance, making it a particularly insidious form of statistical error. As the experimental and statistical issues examined here are common, the insights and solutions we developed will likely impact many fields of biology.

neuroscience↗

Columnar localization and laminar origin of cortical surface electrical potentials

Electrocorticography (ECoG) methodologically bridges basic neuroscience and understanding of human brains in health and disease. However, the localization of ECoG signals across the surface of the brain and the spatial distribution of their generating neuronal sources are poorly understood. To address this gap, we recorded from rat auditory cortex using customized ECoG, and simulated cortical surface electrical potentials with a full-scale, biophysically detailed cortical column model. Experimentally, ECoG-derived auditory representations were tonotopically organized and signals were anisotropically localized to [≤]{+/-}200 m, i.e., a single cortical column. Biophysical simulations reproduce experimental findings, and indicate that neurons in cortical layers V and VI contribute [~]85% of evoked high-gamma signal recorded at the surface. Cell number and synchronicity were the primary biophysical properties determining laminar contributions to evoked ECoG signals, while distance was only a minimal factor. Thus, evoked ECoG signals primarily originate from neurons in the infragranular layers of a single cortical column. In BriefBaratham et al., investigated the localization and origins of sensory evoked ECoG responses. They experimentally found that ECoG responses were anisotropically localized [≤]{+/-}200 m, i.e., a single cortical column. Biophysically detailed simulations revealed that neurons in layers V &VI were the primary sources of evoked ECoG responses, in contrast to common thinking. HighlightsEvoked ECoG signals are localized on the surface to a cortical column. Neurons in cortical layers V and VI constitute the vast majority of the signal recorded at the surface. Different laminar contributions to ECoG signal are driven by cell density and synchronicity.

neuroscience↗

An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro/adipogenic progenitors in fibrodysplasia ossificans progressiva mice

Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease characterized by progressive and catastrophic heterotopic ossification (HO) of skeletal muscle and associated soft tissues. FOP is caused by dominantly acting mutations in the bone morphogenetic protein (BMP) type I receptor, ACVR1 (also known as ALK2), the most prevalent of which is an arginine to histidine substitution [ACVR1(R206H)] in the glycine-serine rich intracellular domain of the receptor. A fundamental pathological consequence of FOP-causing ACVR1 receptor mutations is to enable activin A to initiate canonical BMP signaling in responsive progenitors, which drives skeletogenic commitment and HO. With the clear targets of activin A and ACVR1 identified, development of antibody therapeutics to prevent ligand-receptor interactions is an interventional approach currently being explored. Here, we developed a monoclonal blocking antibody (JAB0505) to the extracellular domain of ACVR1 and tested its ability to inhibit HO in established FOP mouse models. JAB0505 inhibited BMP-dependent gene expression in wild-type and ACVR1(R206H)-overexpressing cell lines. Strikingly, however, JAB0505 treatment markedly exacerbated injury-induced HO in two independent FOP mouse models in which ACVR1(R206H) was either broadly expressed, or more selectively expressed in fibro/adipogenic progenitors (FAPs). JAB0505 drove HO even under conditions of activin A inhibition, indicating that JAB0505 has receptor agonist activity. JAB0505-treated mice exhibited multiple, distinct foci of heterotopic lesions, suggesting an atypically broad anatomical domain of FAP recruitment to endochondral ossification. In addition, skeletogenic differentiation was both delayed and prolonged, and this was accompanied by dysregulation of FAP population growth. Collectively, alterations in the growth and differentiative properties of FAPs and FAP-derived skeletal cells are implicated in the aggravated HO phenotype. These data raise serious safety and efficacy concerns for the use of anti-ACVR1 antibodies to treat FOP patients.

developmental biology↗

The Neurodata Without Borders ecosystem for neurophysiological data science

The neurophysiology of cells and tissues are monitored electrophysiologically and optically in diverse experiments and species, ranging from flies to humans. Understanding the brain requires integration of data across this diversity, and thus these data must be findable, accessible, interoperable, and reusable (FAIR). This requires a standard language for data and metadata that can coevolve with neuroscience. We describe design and implementation principles for a language for neurophysiology data. Our open-source software (Neurodata Without Borders, NWB) defines and modularizes the interdependent, yet separable, components of a data language. We demonstrate NWBs impact through unified description of neurophysiology data across diverse modalities and species. NWB exists in an ecosystem, which includes data management, analysis, visualization, and archive tools. Thus, the NWB data language enables reproduction, interchange, and reuse of diverse neurophysiology data. More broadly, the design principles of NWB are generally applicable to enhance discovery across biology through data FAIRness.

neuroscience↗

NWB:N 2.0: An Accessible Data Standard for Neurophysiology

Neurodata Without Borders: Neurophysiology (NWB:N) is a data standard for neurophysiology, providing neuroscientists with a common standard to share, archive, use, and build common analysis tools for neurophysiology data. With NWB:N version 2.0 (NWB:N 2.0) we made significant advances towards creating a usable standard, software ecosystem, and vibrant community for standardizing neurophysiology data. In this manuscript we focus in particular on the NWB:N data standard schema and present advances towards creating an accessible data standard for neurophysiology.

neuroscience↗

Use of a Neural Circuit Probe to Validate in silico Predictions of Inhibitory Connections

Understanding how neuronal signals propagate in local network is an important step in understanding information processing. As a result, spike trains recorded with Multi-electrode Arrays (MEAs) have been widely used to study behaviors of neural connections. Studying the dynamics of neuronal networks requires the identification of both excitatory and inhibitory connections. The detection of excitatory relationships can robustly be inferred by characterizing the statistical relationships of neural spike trains. However, the identification of inhibitory relationships is more difficult: distinguishing endogenous low firing rates from active inhibition is not obvious. In this paper, we propose an in silico interventional procedure that makes predictions about the effect of stimulating or inhibiting single neurons on other neurons, and thereby gives the ability to accurately identify inhibitory causal relationships. To experimentally test these predictions, we have developed a Neural Circuit Probe (NCP) that delivers drugs transiently and reversibly on individually identified neurons to assess their contributions to the neural circuit behavior. With the help of NCP, three inhibitory connections identified by our in silico modeling were validated through real interventional experiments. Together, these methods provide a basis for mapping complete neural circuits.

neuroscience↗