Neural systems can be modeled as complex networks in which neural elements are represented as nodes linked to one another through structural or functional connections. The resulting network can be analyzed using mathematical tools from network science and graph theory to quantify the system's topological organization and to better understand its function. Here, we used two-photon calcium imaging to record spontaneous activity from the same set of cells in mouse auditory cortex over the course of several weeks. We reconstruct functional networks in which cells are linked to one another by edges weighted according to the correlation of their fluorescence traces. We show that the networks exhibit modular structure across multiple topological scales and that these multi-scale modules unfold as part of a hierarchy. We also show that, on average, network architecture becomes increasingly dissimilar over time, with similarity decaying monotonically with the distance (in time) between sessions. Finally, we show that a small fraction of cells maintain strongly-correlated activity over multiple days, forming a stable temporal core surrounded by a fluctuating and variable periphery. Our work indicates a framework for studying spontaneous activity measured by two-photon calcium imaging using computational methods and graphical models from network science. The methods are flexible and easily extended to additional datasets, opening the possibility of studying cellular level network organization of neural systems and how that organization is modulated by stimuli or altered in models of disease.
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http://dx.doi.org/10.1371/journal.pcbi.1007360 | DOI Listing |
Mutations in the gene cause the most common form of human hereditary hearing loss, known as DFNB1. is expressed in two cell groups of the cochlea-epithelial cells of the organ of Corti and fibrocytes of the inner sulcus and lateral wall-but not by sensory hair cells or neurons. Attempts to treat mouse models of DFNB1 with AAV vectors mediating nonspecific expression have not substantially restored function, perhaps because inappropriate expression in hair cells and neurons could compromise their electrical activity.
View Article and Find Full Text PDFRecent work has claimed that most apparently cross-modal responses in sensory cortex are instead caused by the face movements evoked by stimuli of the non-dominant modality. We show that visual stimuli rarely trigger face movements in awake mice; when they occur, such movements do not explain visual responses in auditory cortex; and in simultaneous recordings, face movements drove artifactual cross-modal responses in visual but not auditory cortex. Thus face movements do not broadly explain cross-modal activity across all stimulus modalities.
View Article and Find Full Text PDFiScience
November 2024
Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Plastic changes in the brain are primarily limited to early postnatal periods. Recovery of adult brain plasticity is critical for the effective development of therapies. A brief (1-2 weeks) duration of visual deprivation (dark exposure, DE) in adult mice can trigger functional plasticity of thalamocortical and intracortical circuits in the primary auditory cortex suggesting improved sound processing.
View Article and Find Full Text PDFJ Neurodev Disord
January 2025
Graduate Neuroscience Program, University of California, Riverside, CA, USA.
Background: Fragile X syndrome (FXS) is a leading known genetic cause of intellectual disability and autism spectrum disorders (ASD)-associated behaviors. A consistent and debilitating phenotype of FXS is auditory hypersensitivity that may lead to delayed language and high anxiety. Consistent with findings in FXS human studies, the mouse model of FXS, the Fmr1 knock out (KO) mouse, shows auditory hypersensitivity and temporal processing deficits.
View Article and Find Full Text PDFNat Commun
January 2025
School of Biosciences, University of Sheffield, Sheffield, S10 2TN, UK.
The refinement of neural circuits towards mature function is driven during development by patterned spontaneous calcium-dependent electrical activity. In the auditory system, this sensory-independent activity arises in the pre-hearing cochlea and regulates the survival and refinement of the auditory pathway. However, the origin and interplay of calcium signals during cochlear development is unknown in vivo.
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