Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.9
3.3
Journals
Brain Sciences
Special Issues
Research on the Etiology of Neurological Disorders Based on Mechanisms...
share announcement

Research on the Etiology of Neurological Disorders Based on Mechanisms of Neuronal Morphogenesis

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 (5 June 2019) | Viewed by 7444

Special Issue Editor

Dr. Kazuhito Toyooka

E-Mail Website
Guest Editor
Department of Neurobiology and Anatomy, Drexel University College of Medicine, 2900 Queen Lane, Philadelphia, PA 19129, USA
Interests: neurodevelopmental disorder; neurodevelopment; brain development; neurite formation; neuronal migration; spine formation; synapse formation; neural connectivity; electrophysiology; behavior; mouse genetics; autism spectrum disorder
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuronal morphogenesis begins at an early embryonic stage during the induction of the neural plate and continues through neonatal development. For example, in the developing brain, after migrating post-mitotic neurons reach the cortical plate in the cerebral cortex, neurons start establishing neuronal circuits. Following neurite formation, dendritic spines and synapses begin to form. Defects in neuronal morphogenesis cause improper neural circuit formation, which has been implicated in neurological disorders. These include a broad range of disorders, such as autism, schizophrenia, epilepsy, and mental retardation.

In this special issue, "Research on the Etiology of Neurological Disorders Based on Mechanisms of Neuronal Morphogenesis" invites researchers to submit their original manuscripts and review articles. We are interested in any topic regarding neuronal morphology, in which defects result in neurological disorders. The goal of this special issue is to further understand the mechanisms of neuronal morphogenesis underlying the pathogenesis of neurological disorders and share the recent advancement of the knowledge and technologies useful for the dissection of the etiology.

Dr. Kazuhito Toyooka
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. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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

  • Neurite formation
  • Neurite initiation
  • Neurite elongation
  • Axon outgrowth
  • Neuritogenesis
  • Dendritic branching
  • Spine formation
  • Spine maturation
  • Synapse formation
  • Synaptogenesis

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

9 pages, 962 KiB  
Article
Comparative Volumetric Analysis of the Brain and Cerebrospinal Fluid in Chiari Type I Malformation Patients: A Morphological Study
by Seckin Aydin and Baris Ozoner
Brain Sci. 2019, 9(10), 260; https://doi.org/10.3390/brainsci9100260 - 29 Sep 2019
Cited by 4 | Viewed by 3127
Abstract
Background: Chiari Type I malformation (CM-I) is defined as the migration of cerebellar tonsils from the foramen magnum in the caudal direction and is characterized by the disproportion of the neural structures. The aim of this study was to investigate the brain volume [...] Read more.
Background: Chiari Type I malformation (CM-I) is defined as the migration of cerebellar tonsils from the foramen magnum in the caudal direction and is characterized by the disproportion of the neural structures. The aim of this study was to investigate the brain volume differences between CM-I patients and normal population using a comparative volumetric analysis. Methods: 140 patients with CM-I and 140 age- and sex-matched healthy controls were included in this study. The magnetic resonance imaging (MRI) data of both groups were analyzed with an automated MRI brain morphometry system. Total intracranial, cerebrum, cerebellum, brainstem, cerebrospinal fluid (CSF), and lateral ventricle volumes as well as cerebrum and cerebellum gray/white matter (GM/WM) volumes were measured. Statistical analysis was performed. Results: Both total CSF and lateral ventricle volumes and volume percentages (Pct) were found significantly higher in CM-I patients compared to the control group. However, there were significant decreases in cerebrum and cerebellum volume Pct in CM-I patients. Although there were no significant differences in cerebrum WM volumes and volume Pct, cerebrum GM volume Pct were found to be significantly lower in CM-I patients. Conclusions: Revealing the increased CSF and lateral ventricle volume, and volume Pct supported concomitant ventricular enlargement and hydrocephalus in some CM-I patients. Decreased cerebrum GM volume Pct compared to the control group might be the underlying factor of some cortical dysfunctions in CM-I patients. Full article
(This article belongs to the Special Issue Research on the Etiology of Neurological Disorders Based on Mechanisms of Neuronal Morphogenesis)
►▼ Show Figures

Figure 1

11 pages, 32018 KiB  
Article
Opposing Morphogenetic Defects on Dendrites and Mossy Fibers of Dentate Granular Neurons in CRMP3-Deficient Mice
by Tam T. Quach, Nathalie Auvergnon, Rajesh Khanna, Marie-Françoise Belin, Papachan E. Kolattukudy, Jérome Honnorat and Anne-Marie Duchemin
Brain Sci. 2018, 8(11), 196; https://doi.org/10.3390/brainsci8110196 - 03 Nov 2018
Cited by 7 | Viewed by 3905
Abstract
Collapsin response mediator proteins (CRMPs) are highly expressed in the brain during early postnatal development and continue to be present in specific regions into adulthood, especially in areas with extensive neuronal plasticity including the hippocampus. They are found in the axons and dendrites [...] Read more.
Collapsin response mediator proteins (CRMPs) are highly expressed in the brain during early postnatal development and continue to be present in specific regions into adulthood, especially in areas with extensive neuronal plasticity including the hippocampus. They are found in the axons and dendrites of neurons wherein they contribute to specific signaling mechanisms involved in the regulation of axonal and dendritic development/maintenance. We previously identified CRMP3’s role on the morphology of hippocampal CA1 pyramidal dendrites and hippocampus-dependent functions. Our focus here was to further analyze its role in the dentate gyrus where it is highly expressed during development and in adults. On the basis of our new findings, it appears that CRMP3 has critical roles both in axonal and dendritic morphogenesis of dentate granular neurons. In CRMP3-deficient mice, the dendrites become dystrophic while the infrapyramidal bundle of the mossy fiber shows aberrant extension into the stratum oriens of CA3. This axonal misguided projection of granular neurons suggests that the mossy fiber-CA3 synaptic transmission, important for the evoked propagation of the activity of the hippocampal trisynaptic circuitry, may be altered, whereas the dystrophic dendrites may impair the dynamic interactions with the entorhinal cortex, both expected to affect hippocampal function. Full article
(This article belongs to the Special Issue Research on the Etiology of Neurological Disorders Based on Mechanisms of Neuronal Morphogenesis)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop