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Molecular Research of Neurotransmitters in Health and Disease
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Molecular Research of Neurotransmitters in Health and Disease

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 June 2023) | Viewed by 4207

Special Issue Editor

Prof. Dr. Wang-Tso Lee

E-Mail Website
Guest Editor
1. Department of Pediatric Neurology, National Taiwan University Children’s Hospital, Taipei 100, Taiwan
2. Graduate Institute of Brain and Mind Sciences, National Taiwan University College of Medicine, Taipei 100, Taiwan
Interests: epilepsy; movement disorders; neurotransmitter diseases; neurometabolic diseases; neurodevelopmental diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurotransmitters are a class of special chemical substances released by nerve endings, which transmit chemical signals in axons through receptors on the innervated neurons or effector cell membranes, thereby mediating the physiological functions and pathological changes of the body. As important substances for information transmission between neurons, neurotransmitters can be divided into several categories according to their chemical structures, such as cholines, amino acids, monoamines and peptides.

Neurotransmitters are chemical signaling substances that are transmitted between nerve cells and between the nervous system and effectors. While maintaining the homeostasis of the nervous system microenvironment, it also plays an important regulatory role in tumorigenesis, neurodegenerative diseases, movement disorders and other diseases. A better understanding of its underlying mechanisms and signal transduction pathways may be helpful in the treatment of these diseases. This special issue, "Molecular Research of Neurotransmitters in Health and Disease," will focus on the molecular mechanisms of neurotransmitters.

Reviews and research papers, covering the molecular aspects of the current trends in the neurotransmitters, are all welcome.

Prof. Dr. Wang-Tso Lee
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

  • neurotransmitter
  • nerve regeneration
  • excitatory neurotransmitter
  • inhibitory neurotransmitter
  • neurodegenerative diseases
  • movement disorders

Published Papers (2 papers)

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Research

11 pages, 2456 KiB  
Article
5-HT1A Receptor Agonist Treatment Partially Ameliorates Rett Syndrome Phenotypes in mecp2-Null Mice by Rescuing Impairment of Neuron Transmission and the CREB/BDNF Signaling Pathway
by Hongmei Dai, Yoshikazu Kitami, Yu-ichi Goto and Masayuki Itoh
Int. J. Mol. Sci. 2022, 23(22), 14025; https://doi.org/10.3390/ijms232214025 - 14 Nov 2022
Viewed by 1340
Abstract
Rett syndrome (RTT) is an X-linked neurodevelopmental disorder caused by mutations in the gene that encodes methyl CpG-binding protein 2 (MECP2) and is characterized by the loss of acquired motor and language skills, stereotypic movements, respiratory abnormalities and autistic features. There has been [...] Read more.
Rett syndrome (RTT) is an X-linked neurodevelopmental disorder caused by mutations in the gene that encodes methyl CpG-binding protein 2 (MECP2) and is characterized by the loss of acquired motor and language skills, stereotypic movements, respiratory abnormalities and autistic features. There has been no effective treatment for this disorder until now. In this study, we used a Mecp2-null (KO) mouse model of RTT to investigate whether repeated intraperitoneal treatment with the 5-HT1A receptor agonist tandospirone could improve the RTT phenotype. The results showed that administration of tandospirone significantly extended the lifespan of Mecp2-KO mice and obviously ameliorated RTT phenotypes, including general condition, hindlimb clasping, gait, tremor and breathing in Mecp2-KO mice. Tandospirone treatment significantly improved the impairment in GABAergic, glutaminergic, dopaminergic and serotoninergic neurotransmission in the brainstem of Mecp2-KO mice. Decreased dopaminergic neurotransmission in the cerebellum of Mecp2-KO mice was also significantly increased by tandospirone treatment. Moreover, RNA-sequencing analysis found that tandospirone modulates the RTT phenotype, partially through the CREB1/BDNF signaling pathway in Mecp2-KO mice. These findings provide a new option for clinical treatment. Full article
(This article belongs to the Special Issue Molecular Research of Neurotransmitters in Health and Disease)
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22 pages, 21818 KiB  
Article
Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a β-Adrenergic Receptor Blocker
by Ravel Ray, Hind Al Khashali, Ben Haddad, Jadziah Wareham, Kai-Ling Coleman, Danyah Alomari, Robert Ranzenberger, Jeffrey Guthrie, Deborah Heyl and Hedeel Guy Evans
Int. J. Mol. Sci. 2022, 23(21), 12829; https://doi.org/10.3390/ijms232112829 - 24 Oct 2022
Cited by 17 | Viewed by 2263
Abstract
It is well-recognized that cigarette smoking is a primary risk factor in the development of non-small cell lung cancer (NSCLC), known to account for ~80% of all lung cancers with nicotine recognized as the major addictive component. In investigating the effect of nicotine, [...] Read more.
It is well-recognized that cigarette smoking is a primary risk factor in the development of non-small cell lung cancer (NSCLC), known to account for ~80% of all lung cancers with nicotine recognized as the major addictive component. In investigating the effect of nicotine, brain-derived neurotrophic factor (BDNF), and the β-adrenergic receptor blocker, propranolol, on sensitivity of NSCLC cell lines, A549 and H1299, to cisplatin, we found increased cell viability, and enhanced cisplatin resistance with nicotine and/or BDNF treatment while opposite effects were found upon treatment with propranolol. Cell treatment with epinephrine or nicotine led to EGFR and IGF-1R activation, effects opposite to those found with propranolol. Blocking EGFR and IGF-1R activation increased cell sensitivity to cisplatin in both cell lines. PI3K and AKT activities were upregulated by nicotine or BDNF and downregulated by cell treatment with inhibitors against EGFR and IGF-1R and by propranolol. Apoptosis and cell sensitivity to cisplatin increased upon co-treatment of cells with cisplatin and inhibitors against PI3K or AKT. Our findings shed light on an interplay between nicotine, BDNF, and β-Adrenergic receptor signaling in regulating survival of lung cancer cells and chemoresistance which can likely expand therapeutic opportunities that target this regulatory network in the future. Full article
(This article belongs to the Special Issue Molecular Research of Neurotransmitters in Health and Disease)
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