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The Regulation of the Cytoskeleton in the Healthy and Diseased Central Nervous System 2.0

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: closed (30 April 2023) | Viewed by 1903

Special Issue Editor


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Guest Editor
Department of Biomedical Sciences, Macquarie University, Sydney, NSW 2109, Australia
Interests: actin cytoskeleton; microtubules; Alzheimer’s disease; motor neuron disease; neurite growth
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The regulation of the cell architecture and particularly the cytoskelelton plays a pivotal role in controlling neuronal connectivity and neuronal function in the central nervous system (CNS). For a long time, changes in the cytoskeletal organisation of neurons has been considered to be largely a byproduct in the pathology of CNS diseases. However, the disruption of the regluatory mechanisms of the cell architecture has been increasingly implicated in the pathogenesis of a large number of neurological and neurodegenerative diseases and CNS injuries, including Alzheimer’s disease, motor neuron disease, epilepsy, schizphrenia, brain trauma and spinal cord injury. Gaining a detailed understanding of the physiological regulation of the cytoskeleton as well as the disease-associated alterations of its regulation will be crucial to develop new therapeutic approaches of dieases that affect the CNS. This Special Issue aims to feature recent advances in the field, of studying the  cytoskeleton in the healthy and dieased nervous system. For this, we are welcoming original resarch article and review contributions, discussing the fundamental regulation of the cytoskeleton in neurons and glial cells in the brain and spinal cord, the molecular basis of disease-associated pathomechanisms of CNS diseases and the use of cytoskeletal building blocks as biomarkers and as drug targets in CNS diseases.

Prof. Dr. Thomas Fath
Guest Editor

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Keywords

  • actin cytoskeleton
  • microtubules
  • intermediate filaments
  • neurodegenerative diseases
  • Alzheimer’ disease
  • motor neuron disease
  • spinal cord injury

Published Papers (1 paper)

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Research

16 pages, 2578 KiB  
Article
Phosphorylation of Neurofilament Light Chain in the VLO Is Correlated with Morphine-Induced Behavioral Sensitization in Rats
by Yu-Xiang Zhang, Yuan-Mei Zhu, Xi-Xi Yang, Fei-Fei Gao, Jie Chen, Dong-Yu Yu, Jing-Qi Gao, Zhen-Nan Chen, Jing-Si Yang, Chun-Xia Yan and Fu-Quan Huo
Int. J. Mol. Sci. 2023, 24(9), 7709; https://doi.org/10.3390/ijms24097709 - 22 Apr 2023
Viewed by 1684
Abstract
Neurofilament light chain (NF-L) plays critical roles in synapses that are relevant to neuropsychiatric diseases. Despite postmortem evidence that NF-L is decreased in opiate abusers, its role and underlying mechanisms remain largely unknown. We found that the microinjection of the histone deacetylase (HDAC) [...] Read more.
Neurofilament light chain (NF-L) plays critical roles in synapses that are relevant to neuropsychiatric diseases. Despite postmortem evidence that NF-L is decreased in opiate abusers, its role and underlying mechanisms remain largely unknown. We found that the microinjection of the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA) into the ventrolateral orbital cortex (VLO) attenuated chronic morphine-induced behavioral sensitization. The microinjection of TSA blocked the chronic morphine-induced decrease of NF-L. However, our chromatin immunoprecipitation (ChIP)-qPCR results indicated that this effect was not due to the acetylation of histone H3-Lysine 9 and 14 binding to the NF-L promotor. In line with the behavioral phenotype, the microinjection of TSA also blocked the chronic morphine-induced increase of p-ERK/p-CREB/p-NF-L. Finally, we compared chronic and acute morphine-induced behavioral sensitization. We found that although both chronic and acute morphine-induced behavioral sensitization were accompanied by an increase of p-CREB/p-NF-L, TSA exhibited opposing effects on behavioral phenotype and molecular changes at different addiction contexts. Thus, our findings revealed a novel role of NF-L in morphine-induced behavioral sensitization, and therefore provided some correlational evidence of the involvement of NF-L in opiate addiction. Full article
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