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The dynamics of signal transmission in neuronal networks remain incompletely understood. In this study, we propose a novel Rulkov neuronal network model that incorporates Q-learning, a reinforcement learning method, to establish efficient signal transmission pathways. Using a simulated neuronal network, we focused on a key parameter that modulates both the intrinsic dynamics of individual neurons and the input signals received from active neighbors. We investigated how variations in this parameter affect signal transmission efficiency by analyzing changes in attenuation rate, as well as the maximum and minimum firing intervals of the start and goal neurons. Our simulations revealed that signal transmission efficiency between distant neurons was significantly impaired in the parameter region, where a chaotic attractor and an attractor of the eight-periodic points are observed to co-exist. A key finding was that low-frequency oscillatory bursts, while failing long-distance transmission, were capable of amplifying signals in neighboring neurons. Furthermore, we observed variation in signal transmission even when individual neuron dynamics remained similar. This variability, despite similar presynaptic activity, is a biologically significant phenomenon, and it is argued that it may contribute to the flexibility and robustness of information processing. These findings are discussed in the context of their biological implications.
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http://dx.doi.org/10.3390/e27080884 | DOI Listing |
Commun Biol
September 2025
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.
Neuronal development and function are orchestrated by a plethora of regulatory mechanisms that control the abundance, localization, interactions, and function of proteins. A key role in this regard is assumed by post-translational protein modifications (PTMs). While some PTM types, such as phosphorylation or ubiquitination, have been explored comprehensively, PTMs involving ubiquitin-like modifiers (Ubls) have remained comparably enigmatic (Ubls).
View Article and Find Full Text PDFNat Commun
September 2025
Department of Physiology, University of Bern, Bern, Switzerland.
Spiking neural networks (SNNs) inherently rely on the timing of signals for representing and processing information. Augmenting SNNs with trainable transmission delays, alongside synaptic weights, has recently shown to increase their accuracy and parameter efficiency. However, existing training methods to optimize such networks rely on discrete time, approximate gradients, and full access to internal variables such as membrane potentials.
View Article and Find Full Text PDFNat Commun
September 2025
Institute of Neurosciences and Medicine, Brain & Behaviour (INM-7), Research Centre Juelich; Wilhelm-Johnen-Straße 1, Juelich, Germany.
Autism is a neurodevelopmental condition associated with altered resting-state brain function. An increased excitation-inhibition ratio is discussed as a pathomechanism but in-vivo evidence of disturbed neurotransmission underlying functional alterations remains scarce. We compare local resting-state brain activity and neurotransmitter co-localizations between autism (N = 405, N = 395) and neurotypical controls (N = 473, N = 474) in two independent cohorts and correlate them with excitation-inhibition changes induced by glutamatergic (ketamine) and GABAergic (midazolam) medication.
View Article and Find Full Text PDFJ Neurosci
September 2025
Department of Neuroscience, University of Connecticut Health Center, Farmington, CT 06030, United States.
Presenilin mutations are the most common cause of familial Alzheimer's disease (FAD), but the mechanisms by which they disrupt neuronal function remain unresolved, particularly in relation to γ-secretase activity. Using , we show that the presenilin ortholog SEL-12 supports synaptic transmission and axonal integrity through a pathway involving the ryanodine receptor RYR-1. Loss-of-function mutations in either or reduce neurotransmitter release and cause neuronal structural defects, with no additional impairment in double mutants, suggesting a shared pathway.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
The Second Department of Gastroenterology, Shengjing Hospital of China Medical University, No. 36, Sanhao Road, Heping District, Shenyang 110000, Liaoning, China. Electronic address:
Purpose: This study aimed to elaborate the mechanism of cuproptosis induced by HO in ulcerative colitis (UC).
Methods: Bioinformatics based on GSE107499, GSE87466, and GSE92415 datasets was performed to screen hub genes related to cuproptosis. In vitro, cell counting kit 8 (CCK8), flow cytometry were applied for detecting cell proliferation and apoptosis.