Neuronal excitability is commonly modeled using different principles at the cellular and population scales, making it difficult to study how microscopic mechanisms shape macroscopic activity. We introduce a spatiotemporal excitatory-inhibitory (EI) model that unifies these scales through a common mixed-feedback architecture. The model retains the conductance-based circuit structure of Hodgkin-Huxley models and describes intrinsic and synaptic currents through memductances whose temporal and spatial voltage dependence encodes dynamics at the relevant scale. In its minimal form, temporal excitability arises from fast excitatory feedback opposed by slower inhibitory feedback, while spatial excitability arises from short-range excitation opposed by longer-range inhibition, recovering the core lateral-inhibition motif of Amari neural fields. We show that combining these mechanisms gives rise to population excitability in strongly heterogeneous populations. In particular, the model generates population spikes that are localized in both space and time and possess population-level scales distinct from those of individual neuronal spikes, despite substantial cell-to-cell parameter variability. We then show that both intrinsic temporal excitability and spatial synaptic feedback are required for coherent mean-field events and robust spatiotemporal population rhythms. Finally, selective modulation of memductances in a subset of the population tunes the frequency of the population rhythm, illustrating how changes at the cellular scale can shape macroscopic dynamics. By separating circuit architecture from modeling scale, the proposed framework provides a physically interpretable approach to analyzing and designing neuronal excitability across scales.
A new mean-field model of a population of Hodgkin–Huxley-type neurons is developed, retaining a microscopic perspective on the ion-exchange mechanisms driving neuronal activity, which allows it to maintain biophysical interpretability while bridging the gap between micro- and macro-scale mechanisms.
G. Rabuffo, Abhirup Bandyopadhyay, Carmela Calabrese et al.· eLife· 0 citations
To understand neural computations, one would like to relate circuit dynamics to neuronal intrinsic excitability and connectivity. We developed tools for large-scale all-optical electrophysiology and applied them to approximately 300 layer 1 interneurons per mouse in vivo. Across two mice, targeted stimulation and volta...
Yitong Ǫi, Vicente J. Parot, Xiang Wu et al.· bioRxiv· 0 citations
Synchronization in networks of conductance-based neurons depends on the external stimulus, coupling architecture, coupling strength, and initial state of the constituent cells. In this work, we numerically investigate a finite all-to-all network of identical Hodgkin–Huxley (HH) neurons coupled through a normalized diff...
Sarbani Das, Saptarshi Das, K. Maharatna· Foundations· 0 citations
Astrocytes are increasingly recognized as active regulators of neural dynamics, yet their role in large-scale synchronization remains incompletely understood. Building on the discovery of breathing cluster synchronization in neuron-astrocyte networks, we investigate whether this phenomenon persists under more biologica...
Ediline L. F. Nguessap, Thierry Njougouo, F. F. Ferreira· 0 citations
Biophysically detailed models of human cortical microcircuit provide key insights into brain function and disease biomarkers, yet their computational cost lengthens simulation runtime and limits scalability. To address this, we systematically evaluated recent simplification methods for morphological reduction and synap...
Cortical circuits must respond flexibly to new inputs while integrating information about the past, yet the way in which neural activity reconciles these competing demands remains unclear. Combining Neuropixels recordings from six mouse visual areas with mechanistic circuit modeling, we identify a dynamical regime in w...
Brendan Harris, Pu-Lin Gong· 0 citations
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