Search bioRxiv⌕ Search

bioRxiv · 10.1101/2022.07.19.500618

A physical neural mass model framework for the analysis of oscillatory generators from laminar electrophysiological recordings

Abstract

Cortical function emerges from the interactions of multi-scale networks that may be studied at a high level using neural mass models (NMM), representing the mean activity of large numbers of neurons. In order to properly reproduce experimental data, these models require the addition of further elements. Here we provide a framework integrating conduction physics that can be used to simulate cortical electrophysiology measurements, particularly those obtained from multi-contact laminar electrodes. This is achieved by endowing NMMs with basic physical properties, such as the average laminar location of the apical and basal dendrites of pyramidal cell populations. We call this framework laminar NMM, or LaNMM for short. We then employ this framework to infer the location of oscillatory generators from laminar-resolved data collected from the prefrontal cortex in the macaque monkey. Based on the literature on columnar connectivity, we define a minimal neural mass model capable of generating amplitude and phase coupled slow (alpha/beta, 4-22 Hz) and fast (gamma, 30-250 Hz) oscillations. The synapse layer locations of the two pyramidal cell populations are treated as optimization parameters, together with two more LaNMM-specific parameters, to compare the models with the multi-contact recordings. We rank the candidate models using an optimization function that evaluates the match between the functional connectivity (FC) of the model and data, where the FC is defined by the covariance between bipolar voltage measurements at different cortical depths. The family of best solutions reproduces the FC of the observed electrophysiology while selecting locations of pyramidal cells and their synapses that result in the generation of fast activity at superficial layers and slow activity across most depths, in line with recent literature proposals. HighlightsO_LIWe provide a neural mass modeling formalism that includes a physical layer to simulate electrophysiology measurements. C_LIO_LITo analyze in-vivo data collected in the macaque monkey during a memory task, we propose a specific model with two coupled main circuits that can generate realistic electrophysiological signals in two important oscillatory regimes--the alpha/beta and the gamma bands. C_LIO_LIPhysical elements in the model shed light on the generation of oscillations in the two regimes and on the relative power distribution of fast and slow oscillatory signals across cortical depth, which we show can be altered by the choice of the reference location or method. C_LIO_LIThe model is contrasted with in-vivo data, with parameters adjusted by matching voltage statistics in the alpha/beta and gamma bands, leading to a solution with slow frequency components generated by synapses spanning most cortical layers and fast oscillations in superficial layers. C_LIO_LIThe resulting formalism provides useful tools and concepts to analyze and model data, with implications for understanding altered oscillatory EEG activity in dementia, Alzheimers disease and other disorders with oscillatory features. C_LI

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sanchez-Todo, R., Bastos, A., Lopez-Sola, E., Mercadal, B., Santarnecchi, E., Miller, E. K., Deco, G., Ruffini, G.. 2022-07-20. A physical neural mass model framework for the analysis of oscillatory generators from laminar electrophysiological recordings. https://doi.org/10.1101/2022.07.19.500618

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Rab10 and Arhgef7 interact to promote axon extension by linking vesicle supply and exocytosis

The formation of functional neural circuits begins with the extension of a single axon by immature neurons. Axon elongation requires an expansion of the plasma membrane that depends on the polarization of vesicle trafficking and exocytosis. It is not completely understood how the increased transport of vesicles into the growing axon is linked to their subsequent insertion into the plasma membrane. An analysis of early stages of neuronal differentiation indicates that an asymmetry in neurite length precedes axon specification and the accumulation of PPVs in the nascent axon. We show that increasing the transport of vesicles in unpolarized neurons is sufficient to promote the extension of additional axons. This effect indicates that an increased supply of vesicles stimulates their subsequent insertion into the membrane to allow neurite growth. The link between vesicle transport and exocytosis is mediated by the interaction of Rab10 with Arhgef7. Rab10 stimulates Arhgef7 activity on PPVs as a GEF for Cdc42b to promote axon extension through exocyst-dependent exocytosis, suggesting that their interaction links the increased supply of PPVs to their exocytosis.

neuroscience↗

Subcellular Spatial Profiling Unveils Links Between Neuritic Plaques with Selective Tau Vulnerability in Alzheimer's Disease

Alzheimer's disease (AD) features widespread extracellular amyloid-{beta} plaques but selective intraneuronal tau accumulation in cortical layers II/III and V, while layer IV remains relatively resistant. Here, we combined subcellular spatial transcriptomics with co-registered A{beta} and pTau immunohistochemistry to determine why neurons exposed to comparable plaque-associated pathology differ in somatic pTau accumulation. Plaque-associated neuritic stress occurred similarly across layers, but layer IV neurons showed attenuated pTau accumulation and reduced somatic expression of a shared neurite-soma stress program involving DCTN1, CALM3, NORAD, and PIN1. Trajectory analysis within layers identified tau-vulnerable and resistant neuronal states implicating calcium signaling, retrograde transport, and lysosomal function. Notably, astrocytic APOE-neuronal LRP1 co-expression increased significantly along the pTau-vulnerable trajectory, and APOE {epsilon}4 was associated with stronger coupling of local plaque pathology to pTau-associated molecular programs. These findings reveal neuronal programs and neuron-glia interactions underlying selective tau vulnerability and resistance in AD, highlighting potential tau-targeting therapeutics.

neuroscience↗

Widespread oscillatory suppression in autism persists in the absence of psychotropic medication.

Purpose: Investigate the neural oscillatory activity associated with autism spectrum disorder (ASD) using electroencephalographic (EEG) recordings in children and adolescents. Compare the corresponding oscillatory power between ASD patients taking psychotropic medication with a drug-naive group. Methods: ASD diagnosis was done using DSM-IV and CARS (Childhood Autism Rating Scale). EEG recordings employed 22 scalp electrodes (10/20 system). ASD vs. neurotypical groups were matched for sex and age (5 females; average age: ~10 years old). We analyzed the resting state (eyes open) EEG power spectrum during ~2-minute recordings. The multitaper FFT method was used to estimate spectral power for the delta, theta, alpha, beta and gamma frequency bands. We pooled together data from several electrodes to compute comprehensive power spectra and assess the oscillatory behavior of macro brain regions. Results: We observed widespread (~4Hz - 20Hz) oscillatory suppression comprising the theta, alpha and beta frequency bands. The most widespread and robust ASD-associated power suppression was in the high theta and alpha bands. Delta and gamma bands showed no significant power change for any of the brain regions studied. Results from a subgroup of patients (N = 9) who never used psychotropics confirmed these findings, indicating that they are not an artifact of medication. Conclusion: Suppression in theta, alpha and beta oscillations may offer insights into the neurophysiological underpinnings of autism and could be used as an accessible and comprehensive tool in ASD diagnosis, regardless of the patients being or not on medication.

neuroscience↗