Mechanisms Underlying Neuronal Network Activity

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1740

Special Issue Editor


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Guest Editor
Laboratorio de Neuromodulación, Instituto de Fisiología, BUAP, Puebla 72570, Mexico
Interests: neurons; brain circuits; NMDA receptors; acetylcholine; excitability; Parkinson’s; schizophrenia; learning; attention

Special Issue Information

Dear Colleagues,

I would like to invite you to review the state of the art in the field of NMDA receptors and how acetylcholine can modulate brain circuits. Recent research findings suggest that acetylcholine can co-activate NMDA receptors. Acetylcholine is produced by Meynert nuclei or in cholinergic interneurons in the basal ganglia, among other cholinergic nuclei in the central nervous system. In general, glycine is proposed as a co-activator. However, in the central nervous system, explicitly in the brain cortex, glycinergic cells are not present. This discrepancy may therefore warrant further investigation. As NMDA receptors have been studied under the assumption that glycine is required for them to function, we invite you to delve deeper and address the following question: what happens if NMDA receptors do not require glycine?

In this regard, we can work together to determine the actions of dopamine and serotonin based on this new approach.

Dr. Jorge Flores-Hernandez
Guest Editor

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Keywords

  • neurons
  • brain circuits
  • NMDA receptors
  • acetylcholine
  • excitability
  • Parkinson’s
  • schizophrenia
  • learning
  • attention

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Published Papers (2 papers)

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Review

22 pages, 1294 KiB  
Review
Injury-Driven Structural and Molecular Modifications in Nociceptors
by Mario García-Domínguez
Biology 2025, 14(7), 788; https://doi.org/10.3390/biology14070788 - 29 Jun 2025
Viewed by 293
Abstract
Peripheral tissue injury initiates a multifaceted cascade of structural and molecular modifications within nociceptors, the primary sensory neurons tasked with detecting noxious stimuli. These alterations play a crucial role in the induction and maintenance of pain states, encompassing acute and chronic pain. Structural [...] Read more.
Peripheral tissue injury initiates a multifaceted cascade of structural and molecular modifications within nociceptors, the primary sensory neurons tasked with detecting noxious stimuli. These alterations play a crucial role in the induction and maintenance of pain states, encompassing acute and chronic pain. Structural remodeling includes alterations in axonal architecture, dendritic morphology, and synaptic connectivity, collectively impacting nociceptor excitability and functional integration. Simultaneously, molecular adaptations comprise the regulation of ion channels, receptor expression, and intracellular signaling pathways, as well as transcriptional reprogramming that modulates nociceptive signaling. This review synthesizes current evidence regarding the cellular and molecular bases of injury-induced plasticity in nociceptors, identifying prospective targets for therapeutic intervention to counteract maladaptive sensitization. Elucidating these processes is critical for the advancement of pain treatment strategies and for enhancing clinical outcomes in individuals experiencing neuropathic pain secondary to tissue injury. Full article
(This article belongs to the Special Issue Mechanisms Underlying Neuronal Network Activity)
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18 pages, 1722 KiB  
Review
The Neural Mechanisms of Visual and Vestibular Interaction in Self-Motion Perception
by Jing Liu and Fu Zeng
Biology 2025, 14(7), 740; https://doi.org/10.3390/biology14070740 - 21 Jun 2025
Viewed by 462
Abstract
Self-motion perception is a complex multisensory process that relies on the integration of various sensory signals, particularly visual and vestibular inputs, to construct stable and unified perceptions. It is essential for spatial navigation and effective interaction with the environment. This review systematically explores [...] Read more.
Self-motion perception is a complex multisensory process that relies on the integration of various sensory signals, particularly visual and vestibular inputs, to construct stable and unified perceptions. It is essential for spatial navigation and effective interaction with the environment. This review systematically explores the mechanisms and computational principles underlying visual–vestibular integration in self-motion perception. We first outline the individual contributions of visual and vestibular cues and then introduce Bayesian inference as a normative framework for the quantitative modeling of multisensory integration. We also discuss multisensory recalibration as a critical mechanism in resolving conflicts between sensory inputs and maintaining perceptual stability. Using heading perception as a model system, we further describe the relevant visual and vestibular pathways involved in this process, as well as the brain regions involved. Finally, we discuss the neural mechanisms mediating visual–vestibular interactions through models of the Bayesian optimal integration and divisive normalization. Full article
(This article belongs to the Special Issue Mechanisms Underlying Neuronal Network Activity)
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