A connectomics-based taxonomy of mammals
Abstract
Mammalian taxonomies are conventionally defined by morphological traits and genetics. How species differ in terms of neural circuits and whether inter-species differences in neural circuit organization conform to these taxonomies is unknown. The main obstacle for the comparison of neural architectures have been differences in network reconstruction techniques, yielding species-specific connectomes that are not directly comparable to one another. Here we comprehensively chart connectome organization across the mammalian phylogenetic spectrum using a common reconstruction protocol. We analyze the mammalian MRI (MaMI) data set, a database that encompasses high-resolution ex vivo structural and diffusion magnetic resonance imaging (MRI) scans of 124 species across 12 taxonomic orders and 5 superorders, collected using a unified MRI protocol. We assess similarity between species connectomes using two methods: similarity of Laplacian eigenspectra and similarity of multiscale topological features. We find greater inter-species similarities among species within the same taxonomic order, suggesting that connectome organization reflects established taxonomic relationships defined by morphology and genetics. While all connectomes retain hallmark global features and relative proportions of connection classes, inter-species variation is driven by local regional connectivity profiles. By encoding connectomes into a common frame of reference, these findings establish a foundation for investigating how neural circuits change over phylogeny, forging a link from genes to circuits to behaviour.
Data availability
The MaMI data set was originally collected and analyzed by Assaf and colleagues in Assaf, Y. et al., 2020 , Nat. Neurosci. (doi: https://doi.org/10.1038/s41593-020-0641-7). We have included the connectivity matrices used in this study in a public repository available at \url{https://doi.org/10.5281/zenodo.7143143}.
Article and author information
Author details
Funding
Natural Sciences and Engineering Research Council of Canada
- Bratislav Misic
National Science Foundation - BSF
- Yaniv Assaf
Canadian Institutes of Health Research
- Bratislav Misic
Fondation Brain Canada (Future Leaders Fund)
- Bratislav Misic
Canada Research Chairs
- Bratislav Misic
Michael J. Fox Foundation for Parkinson's Research
- Bratislav Misic
Healthy Brains for Healthy Lives
- Bratislav Misic
Natural Sciences and Engineering Research Council of Canada
- Guillaume Lajoie
Canada Research Chairs
- Guillaume Lajoie
Canadian Institute for Advanced Research
- Guillaume Lajoie
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2022, Suarez et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 1,783
- views
-
- 291
- downloads
-
- 17
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
- Neuroscience
Substance-induced social behavior deficits dramatically worsen the clinical outcome of substance use disorders; yet, the underlying mechanisms remain poorly understood. Herein, we investigated the role for the corticotropin-releasing factor receptor 1 (CRF1) in the acute sociability deficits induced by morphine and the related activity of oxytocin (OXY)- and arginine-vasopressin (AVP)-expressing neurons of the paraventricular nucleus of the hypothalamus (PVN). For this purpose, we used both the CRF1 receptor-preferring antagonist compound antalarmin and the genetic mouse model of CRF1 receptor-deficiency. Antalarmin completely abolished sociability deficits induced by morphine in male, but not in female, C57BL/6J mice. Accordingly, genetic CRF1 receptor-deficiency eliminated morphine-induced sociability deficits in male mice. Ex vivo electrophysiology studies showed that antalarmin also eliminated morphine-induced firing of PVN neurons in male, but not in female, C57BL/6J mice. Likewise, genetic CRF1 receptor-deficiency reduced morphine-induced firing of PVN neurons in a CRF1 gene expression-dependent manner. The electrophysiology results consistently mirrored the behavioral results, indicating a link between morphine-induced PVN activity and sociability deficits. Interestingly, in male mice antalarmin abolished morphine-induced firing in neurons co-expressing OXY and AVP, but not in neurons expressing only AVP. In contrast, in female mice antalarmin did not affect morphine-induced firing of neurons co-expressing OXY and AVP or only OXY, indicating a selective sex-specific role for the CRF1 receptor in opiate-induced PVN OXY activity. The present findings demonstrate a major, sex-linked, role for the CRF1 receptor in sociability deficits and related brain alterations induced by morphine, suggesting new therapeutic strategy for opiate use disorders.
-
- Evolutionary Biology
- Neuroscience
The first complete 3D reconstruction of the compound eye of a minute wasp species sheds light on the nuts and bolts of size reduction.