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| Home > Publications database > Investigating alpha rhythm generation in a full-density visual thalamocortical model |
| Poster (Other) | FZJ-2023-04362 |
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2023
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Please use a persistent id in citations: doi:10.34734/FZJ-2023-04362
Abstract: Background: The alpha rhythm is a brain oscillation with a frequency around 10 Hz that is predominantly associated with spontaneous ongoing activity and manifests in the occipitoparietal regions of various mammalian species during states of eyes-closed rest. While several hypotheses suggest thalamic and cortical circuits as the primary sources, the exact substrates and mechanisms remain elusive.Objectives: The objective of this study is to present a spiking thalamocortical model to explore potential alpha generator hypotheses. The study investigates two candidate mechanisms for alpha generation: 1) rhythmic bursts around 10 Hz produced by pyramidal neurons in L5 [1]; and 2) a thalamocortical loop delay of approximately 100 ms suggested in previous mean-field models [2].Materials and Methods: The model encompasses the primary visual cortex and the lateral geniculate nucleus. The cortical component represents 1 mm2 of cortical surface. It is partitioned into four layers (L2/3, L4, L5, and L6), each comprising excitatory and inhibitory spiking neurons modeled using the adaptive exponential integrate-and-fire model. The thalamic network, composed of excitatory and inhibitory populations, is simulated with the same neuron model. Thalamocortical connections are established onto cortical neurons in L4 and L6, with reciprocal feedback from L6 neurons to the thalamus. Based on estimated current source density signals from simulated spiking activity, we compared spectra and Granger causality with experimental data. All network simulations were conducted using the NEST simulator. Results and Conclusions: We analyzed the spontaneous activity of the cortical microcircuit and tested the two hypotheses independently within the model. The findings demonstrate that both mechanisms can support alpha oscillations, albeit with distinct laminar patterns. Hypothesis 1 suggests that Granger causality within the alpha range primarily originates from L5 and L2/3, in a pattern resembling top-down propagation from higher cortical areas, as seen experimentally in a previous study [3]. Hypothesis 2 points to L4 and L6 as the main source layers, corresponding to a bottom-up pattern (from thalamus to cortex), similar to the pattern reported in another experimental study [4]. Combining both mechanisms results in a summation of effects, with the alpha oscillation emanating from all layers. The findings suggest that the two mechanisms may contribute differently to alpha rhythms, with distinct laminar patterns, and may be expressed either separately or in tandem under different conditions.
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