Search arXivSearch

arXiv · 2412.01707

The Thermodynamic Model to Study the Slow Afterhyperpolarization in a Single Neuron at Different ATP Levels

Abstract

The neuron consumes energy from ATP hydrolysis to maintain a far-from-equilibrium steady state inside the cell, thus all physiological functions inside the cell are modulated by thermodynamics. The neurons that manage information encoding, transferring, and processing with high energy consumption, displaying a phenomenon called slow afterhyperpolarization after burst firing, whose properties are affected by the energy conditions. Here we constructed a thermodynamical model to quantitatively describe the sAHP process generated by $Na^+-K^+$ ATPases(NKA) and the Calcium-activated potassium(K(Ca)) channels. The model simulates how the amplitude of sAHP is effected by the intracellular ATP concentration and ATP hydrolysis free energy $Δ$ G. The results show a trade-off between NKA and the K(Ca)'s modulation on the sAHP's energy dependence, and also predict an alteration of sAHP's behavior under insufficient ATP supply if the proportion of NKA and K(Ca)'s expression quantities is changed. The research provides insights in understanding the maintenance of neural homeostasis and support furthur researches on metabolism-related and neurodegenerative diseases.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Jianwei Li, Simeng Yu, Mingye Guo, Xuewen Shen, Qi Ouyang, Fangting Li. 2024-12-02. The Thermodynamic Model to Study the Slow Afterhyperpolarization in a Single Neuron at Different ATP Levels. https://arxiv.org/abs/2412.01707

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

KEEP EXPLORING

Related papers

Improving the adaptive and continuous learning capabilities of artificial neural networks: Lessons from multi-neuromodulatory dynamics

Continuous adaptive learning, the ability to adapt to the environment and keep improving performance, is a hallmark of natural intelligence. Biological organisms excel in acquiring, transferring, and retaining knowledge while adapting to volatile environments, making them a source of inspiration for artificial neural networks (ANNs). This study explores how neuromodulation, a building block of learning in biological systems, can help address catastrophic forgetting and enhance the robustness of ANNs in continual learning. Driven by neuromodulators including dopamine (DA), acetylcholine (ACh), serotonin (5-HT) and noradrenaline (NA), neuromodulatory processes in the brain operate at multiple scales, facilitating dynamic responses to environmental changes through mechanisms ranging from local synaptic plasticity to global network-wide adaptability. Importantly, the relationship between neuromodulators and their interplay in modulating sensory and cognitive processes is more complex than previously expected, demonstrating a "many-to-many" neuromodulator-to-task mapping. To inspire neuromodulation-aware learning rules, we highlight (i) how multi-neuromodulatory interactions enrich single-neuromodulator-driven learning, (ii) the impact of neuromodulators across multiple spatio-temporal scales, and correspondingly, (iii) strategies for approximating and integrating neuromodulated learning processes in ANNs, and (iv) an architectural-general formulation of multi-neuromodulatory dynamics. We also present a conceptual study to showcase how neuromodulation-inspired mechanisms, such as DA-driven reward processing and NA-based cognitive flexibility, can enhance ANN performance in a Go/No-Go task. Though multi-scale neuromodulation, we aim to bridge the gap between biological and artificial learning, paving the way for ANNs with greater flexibility, robustness, and adaptability.

q-bio.NC

Axonal delay dispersion decides whether a neuron detects an event or a sequence, and predicts cortical column diameter

Cortical neurons fire sparsely -- often fewer than one spike per sensory window -- making rate coding insufficient and temporal coding a necessity. That conduction delays convert firing order into synchrony is long established. What governs which class of temporal feature a neuron detects -- one volley of coincident input, or two in a particular order -- has not been examined. We propose a delay-signature framework in which the axonal conduction delays converging on a dendritic branch constitute a physical key: only input sequences whose spike-time differences the delays compensate arrive synchronously, and coincidence detection, via calcium plateau thresholds, converts that synchrony into an all-or-none output. In simulations of an integrator-neuron model we report three results. First, a single physical scalar -- the dispersion of the delay set -- moves a population from event detection to order-selective sequence detection. The transition is emergent under random delays and connectivity: at narrow dispersion sequence detectors do not exist, and the dispersion at which they overtake event detectors tracks the inter-event interval with a slope statistically indistinguishable from one. This maps a computational distinction onto the anatomical one between myelinated and unmyelinated projections, making myelination a switch on what a neuron computes, not only a regulator of speed. Second, the same dispersion sets the code's limits: it bounds the longest codable interval and fixes an absolute timing tolerance of about a millisecond, with slowing better tolerated than speeding. Third, that millisecond window and horizontal conduction velocity together predict cortical column diameter, and the two areas with direct measurements fall where the relation puts them. One anatomically measurable parameter thus sets what a neuron detects and the limits of what it can represent.

q-bio.NC

A Roadmap for MEG Foundation Models

Foundation models are beginning to reshape brain-signal analysis by moving the field beyond task-specific decoding pipelines toward reusable models pretrained on broad neural datasets. Magnetoencephalography (MEG) is a compelling but still underdeveloped target for this shift: it captures human cortical dynamics at millisecond resolution while offering stronger spatial interpretability than EEG, making it especially valuable for source-resolved studies of perception, language, cognition, and clinical brain function. Yet MEG foundation models remain at an early stage, with only a small number of MEG-specific and MEG-inclusive multi-modal models, modest pretraining corpora, and emerging but still limited benchmarks. This perspective lays down the basic concepts needed to understand MEG foundation models and provides a didactic overview of the field's key design choices, including tokenization, sensor- versus source-space representations, sensor-geometry encoding, backbone architectures, self-supervised objectives, and pretraining data. We then offer a roadmap for future development, organized around native MEG pretraining, adaptation of EEG foundation models, transfer from generic time-series models, and multi-modal integration with EEG, fMRI, MRI, behaviour, and stimulus features. We highlight the need for coordinated infrastructure, including diverse and reusable MEG datasets, rigorous evaluation across subjects, sites, tasks, and clinical settings, and responsible data-sharing practices that address consent, privacy, access, and governance.

q-bio.NC