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Special Issue "Advances in the Research of Neural Circuits"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 28 February 2023 | Viewed by 2339

Special Issue Editor

Prof. Dr. Masahito Yamagata
E-Mail Website
Guest Editor
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
Interests: neural circuit formation; synapse formation; adhesion molecule; extracellular matrix; connectomics; synthetic biology; genome editing; cell atlas; visual system in birds and mice
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The neuron is a fundamental component of brain function. However, neurons do not function individually—rather, they function through synaptically connected neural circuits and their networks, more recently known as the connectome. Unraveling the structure and function of neural circuits and connectomes requires the combination of various approaches, including biology, chemistry, physics, mathematics, engineering, information technology, clinical medicine, and psychology. In particular, there is no doubt that a panoply of molecular studies and tools have been at the center of this research. For example, biochemical, immunohistochemical, pharmacological, physiological, and genetical studies of synaptic molecules have revealed the roles of those components in the operation of distinct neural circuits as well as their unexpected anatomy and functions. In addition, new tools for connectomics such as traceable molecular reporters, caged compounds, recombinant viruses, calcium indicators, and optogenetics have opened new avenues to examine diverse neural circuits. These technical breakthroughs have helped to understand the neural development and the brain pathology of human aging.

This Special Issue welcomes original and review articles that demonstrate or summarize recent progress in the studies of any neural circuits, with a particular focus on molecular workforces and tools such as proteins, glycoconjugates, neurotransmitters, and lipids.

Prof. Dr. Masahito Yamagata
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • synapse
  • connectome
  • synaptic vesicle
  • synaptic cleft
  • postsynaptic density
  • axon
  • dendrite
  • aging
  • plasticity
  • neuropharmacology

Published Papers (2 papers)

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Research

Article
c-Abl Tyrosine Kinase Is Required for BDNF-Induced Dendritic Branching and Growth
Int. J. Mol. Sci. 2023, 24(3), 1944; https://doi.org/10.3390/ijms24031944 - 18 Jan 2023
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Abstract
Brain-derived neurotrophic factor (BDNF) induces activation of the TrkB receptor and several downstream pathways (MAPK, PI3K, PLC-γ), leading to neuronal survival, growth, and plasticity. It has been well established that TrkB signaling regulation is required for neurite formation and dendritic arborization, but the [...] Read more.
Brain-derived neurotrophic factor (BDNF) induces activation of the TrkB receptor and several downstream pathways (MAPK, PI3K, PLC-γ), leading to neuronal survival, growth, and plasticity. It has been well established that TrkB signaling regulation is required for neurite formation and dendritic arborization, but the specific mechanism is not fully understood. The non-receptor tyrosine kinase c-Abl is a possible candidate regulator of this process, as it has been implicated in tyrosine kinase receptors’ signaling and trafficking, as well as regulation of neuronal morphogenesis. To assess the role of c-Abl in BDNF-induced dendritic arborization, wild-type and c-Abl-KO neurons were stimulated with BDNF, and diverse strategies were employed to probe the function of c-Abl, including the use of pharmacological inhibitors, an allosteric c-Abl activator, and shRNA to downregulates c-Abl expression. Surprisingly, BDNF promoted c-Abl activation and interaction with TrkB receptors. Furthermore, pharmacological c-Abl inhibition and genetic ablation abolished BDNF-induced dendritic arborization and increased the availability of TrkB in the cell membrane. Interestingly, inhibition or genetic ablation of c-Abl had no effect on the classic TrkB downstream pathways. Together, our results suggest that BDNF/TrkB-dependent c-Abl activation is a novel and essential mechanism in TrkB signaling. Full article
(This article belongs to the Special Issue Advances in the Research of Neural Circuits)
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Article
Expansion-Based Clearing of Golgi-Cox-Stained Tissue for Multi-Scale Imaging
Int. J. Mol. Sci. 2022, 23(7), 3575; https://doi.org/10.3390/ijms23073575 - 25 Mar 2022
Viewed by 1412
Abstract
Obtaining fine neuron morphology and connections data is extraordinarily useful in understanding the brain’s functionality. Golgi staining is a widely used method for revealing neuronal morphology. However, Golgi-Cox-stained tissue is difficult to image in three dimensions and lacks cell-type specificity, limiting its use [...] Read more.
Obtaining fine neuron morphology and connections data is extraordinarily useful in understanding the brain’s functionality. Golgi staining is a widely used method for revealing neuronal morphology. However, Golgi-Cox-stained tissue is difficult to image in three dimensions and lacks cell-type specificity, limiting its use in neuronal circuit studies. Here, we describe an expansion-based method for rapidly clearing Golgi-Cox-stained tissue. The results show that 1 mm thick Golgi-Cox-stained tissue can be cleared within 6 hours with a well preserved Golgi-Cox-stained signal. At the same time, we found for the first time that the cleared Golgi-Cox-stained samples were compatible with three-dimensional (3D) immunostaining and multi-round immunostaining. By combining the Golgi-Cox staining with tissue clearing and immunostaining, Golgi-Cox-stained tissue could be used for large-volume 3D imaging, identification of cell types of Golgi-Cox-stained cells, and reconstruction of the neural circuits at dendritic spines level. More importantly, these methods could also be applied to samples from human brains, providing a tool for analyzing the neuronal circuit of the human brain. Full article
(This article belongs to the Special Issue Advances in the Research of Neural Circuits)
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