Réseaux auditifs modifiés à l’échelle de l’ensemble du cerveau dans un modèle de syndrome de l’X fragile chez le poisson-zèbre

Titre original en anglais : Altered brain-wide auditory networks in a zebrafish model of fragile X syndrome

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Constantin, L., Poulsen, R., Scholz, L. A., Favre‐Bulle, I. A., Taylor, M. A., Sun, B., Goodhill, G. J., Vanwalleghem, G., & Scott, E. K. (2020). Altered brain-wide auditory networks in a zebrafish model of fragile X syndrome. BMC Biology, 18(1), 125-125. https://doi.org/10.1186/s12915-020-00857-6

Date de publication: 16/09/2020 Ajout dans AutiHub: 05/07/2026 Type: Article Langue de l’article: Anglais
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Auteurs

Auteur·ices des publications
9
Auteur·ices de la publication identifié·es comme autistes
1 / 9 (11,1 %)
  1. Lena Constantin
  2. Rebecca Poulsen *
  3. Leandro A. Scholz
  4. Itia A. Favre‐Bulle
  5. Michael A. Taylor
  1. Biao Sun
  2. Geoffrey J. Goodhill
  3. Gilles Vanwalleghem
  4. Ethan K. Scott

Résumé

Résumé Contexte La perte ou l’expression perturbée du gène FMR1 provoque le syndrome de l’X fragile (FXS), la forme monogénique d’autisme la plus fréquente chez l’humain. Bien que les perturbations du traitement sensoriel soient des caractéristiques essentielles du FXS et de l’autisme, les fondements neuronaux de ces phénotypes sont mal compris. En utilisant l’imagerie calcique pour enregistrer l’ensemble du cerveau à résolution cellulaire, nous avons étudié les réponses neuronales à des stimuli visuels et auditifs chez des larves de poisson-zèbre, en utilisant des mutants fmr1 pour modéliser le FXS. Le but de cette étude était de modéliser les altérations des réseaux sensoriels, à l’échelle de l’ensemble du cerveau et à résolution cellulaire, qui sous-tendent les aspects sensoriels du FXS et de l’autisme. Résultats En combinant des analyses fonctionnelles avec les positions anatomiques des neurones, nous avons constaté que les animaux fmr1 −/− présentent des réponses normales au mouvement visuel. Cependant, plusieurs altérations étaient présentes dans le traitement auditif des animaux fmr1 −/−. Les réponses auditives étaient plus nombreuses dans les structures du cerveau postérieur et dans le thalamus. Le thalamus, le torus semicircularis et le tegmentum présentaient des amas de neurones qui répondaient plus fortement aux stimuli auditifs chez les animaux fmr1 −/−. Les réseaux de connectivité fonctionnelle montraient une plus grande connectivité interrégionale à de plus faibles intensités sonores (un décalage de − 3 à − 6 dB) chez les larves fmr1 −/− comparativement au type sauvage. Enfin, les capacités de décodage de composantes spécifiques de la voie auditive ascendante étaient modifiées : le noyau octavolatéral du cerveau postérieur présentait un décodage significativement plus fort de l’amplitude auditive, tandis que le télencéphale présentait un décodage plus faible chez les mutants fmr1 −/−. Conclusions Nous avons démontré que les larves fmr1 −/− sont hypersensibles au son, avec un décalage de sensibilité de 3–6 dB, et avons identifié quatre régions cérébrales sous-corticales présentant des réponses plus nombreuses et/ou des forces de réponse plus élevées aux stimuli auditifs. Nous avons également construit un modèle étayé expérimentalement de la manière dont l’information auditive pourrait être traitée à l’échelle de l’ensemble du cerveau chez les larves fmr1 −/−. Notre modèle suggère que la voie auditive ascendante précoce transmet davantage d’information auditive, avec moins de filtrage et de modulation, dans ce modèle de FXS.

Abstract Background Loss or disrupted expression of the FMR1 gene causes fragile X syndrome (FXS), the most common monogenetic form of autism in humans. Although disruptions in sensory processing are core traits of FXS and autism, the neural underpinnings of these phenotypes are poorly understood. Using calcium imaging to record from the entire brain at cellular resolution, we investigated neuronal responses to visual and auditory stimuli in larval zebrafish, using fmr1 mutants to model FXS. The purpose of this study was to model the alterations of sensory networks, brain-wide and at cellular resolution, that underlie the sensory aspects of FXS and autism. Results Combining functional analyses with the neurons’ anatomical positions, we found that fmr1 −/− animals have normal responses to visual motion. However, there were several alterations in the auditory processing of fmr1 −/− animals. Auditory responses were more plentiful in hindbrain structures and in the thalamus. The thalamus, torus semicircularis, and tegmentum had clusters of neurons that responded more strongly to auditory stimuli in fmr1 −/− animals. Functional connectivity networks showed more inter-regional connectivity at lower sound intensities (a − 3 to − 6 dB shift) in fmr1 −/− larvae compared to wild type. Finally, the decoding capacities of specific components of the ascending auditory pathway were altered: the octavolateralis nucleus within the hindbrain had significantly stronger decoding of auditory amplitude while the telencephalon had weaker decoding in fmr1 −/− mutants. Conclusions We demonstrated that fmr1 −/− larvae are hypersensitive to sound, with a 3–6 dB shift in sensitivity, and identified four sub-cortical brain regions with more plentiful responses and/or greater response strengths to auditory stimuli. We also constructed an experimentally supported model of how auditory information may be processed brain-wide in fmr1 −/− larvae. Our model suggests that the early ascending auditory pathway transmits more auditory information, with less filtering and modulation, in this model of FXS.

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Ces indicateurs décrivent la bibliographie citée importée pour cette publication. Les métriques de références citées utilisent le total des références citées comme dénominateur. Les métriques d’auteurices cité·es indiquent si elles utilisent toutes les occurrences d’auteurices cité·es ou seulement les occurrences rattachées à des auteurices déjà intégré·es à la base de données AutiHub. Ils utilisent les rattachements mis en cache entre les auteurices cité·es et les auteurices intégré·es à la base de données AutiHub. Dernier calcul : 16/08/2026 11:30.

Références citées
76
Nombre total de références citées intégrées pour cette publication.
Références citées avec un·e auteur·ice identifié·e comme autiste
3 / 76 (3,9 %)
Occurrences d’auteur·ices cité·es identifié·es comme autistes
3 / 457 (0,7 %)
Parmi les occurrences rattachées à des auteurices intégré·es à la base de données AutiHub : 3 / 71 (4,2 %). Auteurices cité·es distinct·es identifié·es comme autistes : 1 / 390 (0,3 %).
Occurrences citées rattachées à la base AutiHub
71 / 457 (15,5 %)
Auteurices cité·es distinct·es rattaché·es : 30 / 390 (7,7 %)
Occurrences rattachées, non identifiées comme autistes
68 / 71 (95,8 %)
Parmi les seules occurrences rattachées. Sur l’ensemble des occurrences d’auteurices cité·es : 68 / 457 (14,9 %). Auteurices cité·es distinct·es rattaché·es, non identifié·es comme autistes : 29 / 30 (96,7 %).
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