Search bioRxivSearch

bioRxiv · 10.1101/2021.03.13.435181

Symmetry processing in the macaque visual cortex

Abstract

Symmetry is a highly salient feature of the natural world that is perceived by many species of the animal kingdom and that impacts a large array of behaviours such as partner selection or food choice. In humans, the cerebral areas processing symmetry are now well identified from neuroimaging measurements. However, we currently lack an animal model to explore the underlying neural mechanisms. Macaque is a potentially good candidate, but a previous comparative study (1) found that functional magnetic resonance imaging (fMRI) responses to mirror symmetry in this species were substantially weaker than those observed in humans under similar experimental conditions. Here, we re-examined symmetry processing in macaques from a broader perspective, using both rotation (experiment 1) and reflection (experiment 2) symmetry. Our experimental design was directly derived from that of a previous human fMRI study (2), in order to facilitate the comparison between the two primate species. Highly consistent responses to symmetry were found in a large network of areas (notably V3, V3A, V4, V4A and PITd), in line with what has been observed in humans. Within this network, response properties in areas V3 and V4 (notably their dependency on the rotation symmetry order) were strikingly similar to those observed in their human counterparts. Our results suggest that the cortical networks that process symmetry in humans and macaques are much more similar than previously reported and point toward macaque as a relevant model for understanding symmetry processing. Significance statementSymmetry processing is an important aspect of human visual perception. We currently lack an animal model for characterizing the neural mechanisms that underlie it at the microscopic scale. Here, we use fMRI measurements in macaques to demonstrate that the cortical responses to symmetry in this species are comparable to those observed in humans under similar experimental conditions to a much higher extent than previously documented. Our results call for a re-examination of the relevance of the macaque model for symmetry processing in humans and open the door to an exploration of the underlying neural mechanisms at the single-cell level, notably in V3, an area often neglected in most current models of visual processing.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Audurier, P., Hejja-Brichard, Y., De Castro, V., Kohler, P. J., Norcia, A., Durand, J.-B., Cottereau, B. R.. 2021-03-13. Symmetry processing in the macaque visual cortex. https://doi.org/10.1101/2021.03.13.435181

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