Structure and Function of Brain Circuits and Networks

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 2687

Special Issue Editors


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Guest Editor
Department of Anatomy and Neurobiology, The University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: neural circuit; mouse behavior; psychiatric disorders; synaptic transmission and plasticity; learning and memory

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Guest Editor
Department of Pharmacology and Physiology, School of Medicine and Health Sciences, The George Washington University, Washington, DC 20037, USA
Interests: machine learning; neural circuit coding of behavior; neural ensemble activity; neurological disorders; systems neuroscience

Special Issue Information

Dear Colleagues,

Welcome to this Special Issue of the journal Brain Sciences, which is dedicated to exploring the intricate world of brain circuits and networks. The brain's complexity lies in its network of interconnected cells that enable our thoughts, emotions, and actions. Understanding the structure and function of these circuits is crucial for unraveling the mysteries of the mind and advancing neuroscience.

This Special Issue brings together cutting-edge research that investigates various aspects of neural connectivity, from microscopic organization to large-scale dynamics. Contributors employ innovative techniques and computational approaches to provide new insights into the principles governing brain function. Topics covered include synaptic plasticity, neural development, information processing, and the role of circuits in cognition and behavior. By examining the interplay between structure and function, we deepen our understanding of neural circuitry and its implications for neurological and psychiatric disorders. We invite readers to explore this collection and embark on a journey through the remarkable world of brain circuits and networks.

Dr. Jianyang Du
Dr. Hui Lu
Guest Editors

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Keywords

  • brain circuits
  • neural networks
  • synaptic plasticity
  • neural development
  • network dynamics
  • neural coding
  • information processing
  • neuron–glia interaction
  • behavioral output
  • neurological disorders

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Published Papers (2 papers)

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Research

15 pages, 2079 KiB  
Article
Stimulation of Dopamine D4 Receptors in the Nucleus Accumbens Shell Increases Palatable Food Intake in Satiated Male Rats: Modulation by NMDA and AMPA Receptors
by Refugio Cruz-Trujillo, Daniel Díaz-Urbina, José Alfredo Díaz-Gandarilla, Dolores Guadalupe Vidal-López, Rodrigo Erick Escartín-Pérez, Juan Manuel Mancilla-Diaz, Benjamín Florán and Juan Gabriel Tejas-Juárez
Brain Sci. 2024, 14(11), 1103; https://doi.org/10.3390/brainsci14111103 - 30 Oct 2024
Viewed by 807
Abstract
Background/Objectives: Palatability significantly influences food consumption, often leading to overeating and obesity by activating the brain’s reward systems. The nucleus accumbens (NAc) plays a central role in this process, modulating reward mechanisms primarily via dopamine through D2-like receptors (D2R, D3R, D4R). While the [...] Read more.
Background/Objectives: Palatability significantly influences food consumption, often leading to overeating and obesity by activating the brain’s reward systems. The nucleus accumbens (NAc) plays a central role in this process, modulating reward mechanisms primarily via dopamine through D2-like receptors (D2R, D3R, D4R). While the involvement of D2 receptors in feeding is well-documented, the role of D4 receptors (D4Rs) is less clear. Methods: Male Wistar rats received intra-NAc shell microinjections of the D4R agonist PD-168077 and the antagonist L-745870. This study also examined the modulation between D4R and glutamatergic transmission by administration of NMDA, NMDA receptor antagonist AP-5, AMPA, and AMPA receptor antagonist CNQX. Results: PD-168077 increased sweet solution intake by 46%, an effect that was reversed by L-745870. Pre-treatment with NMDA prevented the stimulatory effect of PD-168077, whereas the NMDA receptor antagonist AP-5 had no such effect. Additionally, AMPA administration reduced sweet solution intake by 63%, counteracting the effect of PD-168077, while the AMPA receptor antagonist CNQX, on its own, increased intake by 40%. Conclusions: These findings suggest that D4Rs promote hedonic feeding by modulating glutamatergic transmission in the NAc shell, highlighting the complexity of D4R involvement in food intake regulation. This study underscores the potential of targeting D4Rs for therapeutic interventions in eating disorders and obesity, though further research is essential to clarify the precise mechanisms through which D4R modulates AMPA and NMDA receptor activity in feeding behavior. Full article
(This article belongs to the Special Issue Structure and Function of Brain Circuits and Networks)
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14 pages, 2627 KiB  
Article
Acid-Sensing Ion Channel 1a Contributes to the Prefrontal Cortex Ischemia-Enhanced Neuronal Activities in the Amygdala
by Gyeongah Park, Qian Ge, Zhen Jin and Jianyang Du
Brain Sci. 2023, 13(12), 1684; https://doi.org/10.3390/brainsci13121684 - 7 Dec 2023
Cited by 1 | Viewed by 1401
Abstract
Following a stroke, the emergence of amygdala-related disorders poses a significant challenge, with severe implications for post-stroke mental health, including conditions such as anxiety and depression. These disorders not only hinder post-stroke recovery but also elevate mortality rates. Despite their profound impact, the [...] Read more.
Following a stroke, the emergence of amygdala-related disorders poses a significant challenge, with severe implications for post-stroke mental health, including conditions such as anxiety and depression. These disorders not only hinder post-stroke recovery but also elevate mortality rates. Despite their profound impact, the precise origins of aberrant amygdala function after a stroke remain elusive. As a target of reduced brain pH in ischemia, acid-sensing ion channels (ASICs) have been implicated in synaptic transmission after ischemia, hinting at their potential role in reshaping neural circuits following a stroke. This study delves into the intriguing relationship between post-stroke alterations and ASICs, specifically focusing on postsynaptic ASIC1a enhancement in the amygdala following prefrontal cortex (PFC) ischemia induced by endothelin-1 (ET-1) injection. Our findings intriguingly illustrate that mPFC ischemia not only accentuates the PFC to the amygdala circuit but also implicates ASIC1a in fostering augmented synaptic plasticity after ischemia. In contrast, the absence of ASIC1a impairs the heightened induction of long-term potentiation (LTP) in the amygdala induced by ischemia. This pivotal research introduces a novel concept with the potential to inaugurate an entirely new avenue of inquiry, thereby significantly enhancing our comprehension of the intricate mechanisms underlying post-stroke neural circuit reconfiguration. Importantly, these revelations hold the promise of paving the way for groundbreaking therapeutic interventions. Full article
(This article belongs to the Special Issue Structure and Function of Brain Circuits and Networks)
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