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Neurotransmitters in Neurodegenerative Diseases

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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 January 2024) | Viewed by 4230

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Special Issue Editors

Dr. Ryoma Morigaki

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Guest Editor

Department of Advanced Brain Research, Institute of Biomedical Sciences, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan
Interests: basal ganglia; striatum; striosome and matrix; deep brain stimulation; Parkinson’s disease; dystonia
Special Issues, Collections and Topics in MDPI journals

Dr. Helen N. Schwerdt

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Guest Editor

Department of Bioengineering, Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA 15261, USA
Interests: dopamine; basal ganglia; striatum; Parkinson’s disease; neurochemical signaling; electrochemical recording; fast scan cyclic voltammetry; brain implantable devices

Special Issue Information

Dear Colleagues,

Recently, beta-band local field potential measurements from the subthalamic nucleus or globus pallidus internus have been used as diagnostic biomarker metrics for deep brain stimulation therapy and closed-loop stimulation based on the inverse relationship observed between beta-band signaling amplitudes and motor dysfunction in patients with Parkinson’s disease. Advances in biosensing and microfabrication technology, e.g., fast-scan cyclic voltammetry, or other chemical sensing techniques have enabled the direct detection of various neurotransmitters, such as dopamine, serotonin, adenosine, and histamine, in vivo.

The aim of this special issue is to gather review articles and studies related to various neurotransmitters for updating the current understanding of the neurobiology of neurodegenerative disease and to discern molecular signatures of pathology that could be useful for diagnosis and targeted therapeutic (e.g. pharmacological and/or invasive intracranial devices) interventions in the future. Articles related to cutting-edge technologies for detecting or stimulating specific neurotransmitter systems are also accepted to elucidate the current technical resources as well as identify remaining barriers towards translation for clinical use.

Dr. Ryoma Morigaki
Dr. Helen N. Schwerdt
Guest Editors

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

neurotransmitters
basal ganglia
neurodegenerative disease
Parkinson’s disease
neuromodulators
neuroengineering
microfabrication
neurochemicals
neurochemical sensing
electrochemical recording
aptamer
microdialysis
fluid sampling
biomarkers

Published Papers (3 papers)

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Research

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16 pages, 1971 KiB

Open AccessArticle

Memantine Improves the Disturbed Glutamine and γ-Amino Butyric Acid Homeostasis in the Brain of Rats Subjected to Experimental Autoimmune Encephalomyelitis

by Beata Dąbrowska-Bouta, Lidia Strużyńska, Marta Sidoryk-Węgrzynowicz and Grzegorz Sulkowski

Int. J. Mol. Sci. 2023, 24(17), 13149; https://doi.org/10.3390/ijms241713149 - 24 Aug 2023

Cited by 1 | Viewed by 871

Abstract

Glutamine (Gln), glutamate (Glu), and γ-amino butyric acid (GABA) are essential amino acids for brain metabolism and function. Astrocyte-derived Gln is the precursor for the two most important neurotransmitters in the central nervous system (CNS), which are the excitatory neurotransmitter Glu and the inhibitory neurotransmitter GABA. In addition to their roles in neurotransmission, these amino acids can be used as alternative substrates in brain metabolism that enable metabolic coupling between astrocytes and neurons in the glutamate–glutamine cycle (GGC). The disturbed homeostasis of these amino acids within the tripartite synapse may be involved in the pathogenesis of various neurological diseases. Interactions between astrocytes and neurons in terms of Gln, Glu, and GABA homeostasis were studied in different phases of experimental allergic encephalomyelitis (EAE) in Lewis rats. The results of the study showed a decrease in the transport (uptake and release) of Gln and GABA in both neuronal and astrocyte-derived fractions. These effects were fully or partially reversed when the EAE rats were treated with memantine, a NMDA receptor antagonist. Changes in the expression and activity of selected glutamine/glutamate metabolizing enzymes, such as glutamine synthase (GS) and phosphate-activated glutaminase (PAG), which were affected by memantine, were observed in different phases of EAE. The results suggested perturbed homeostasis of Gln, Glu, and GABA during EAE, which may indicate alterations in neuron–astrocyte coupling and dysfunction of the tripartite synapse. Memantine appears to partially regulate the disturbed relationships between Gln, Glu, and GABA. Full article

(This article belongs to the Special Issue Neurotransmitters in Neurodegenerative Diseases)

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30 pages, 5441 KiB

Open AccessArticle

Influence of the Peripheral Nervous System on Murine Osteoporotic Fracture Healing and Fracture-Induced Hyperalgesia

by Isabel Wank, Tanja Niedermair, Daniel Kronenberg, Richard Stange, Christoph Brochhausen, Andreas Hess and Susanne Grässel

Int. J. Mol. Sci. 2023, 24(1), 510; https://doi.org/10.3390/ijms24010510 - 28 Dec 2022

Cited by 1 | Viewed by 1743

Abstract

Osteoporotic fractures are often linked to persisting chronic pain and poor healing outcomes. Substance P (SP), α-calcitonin gene-related peptide (α-CGRP) and sympathetic neurotransmitters are involved in bone remodeling after trauma and nociceptive processes, e.g., fracture-induced hyperalgesia. We aimed to link sensory and sympathetic signaling to fracture healing and fracture-induced hyperalgesia under osteoporotic conditions. Externally stabilized femoral fractures were set 28 days after OVX in wild type (WT), α-CGRP- deficient (α-CGRP −/−), SP-deficient (Tac1−/−) and sympathectomized (SYX) mice. Functional MRI (fMRI) was performed two days before and five and 21 days post fracture, followed by µCT and biomechanical tests. Sympathectomy affected structural bone properties in the fracture callus whereas loss of sensory neurotransmitters affected trabecular structures in contralateral, non-fractured bones. Biomechanical properties were mostly similar in all groups. Both nociceptive and resting-state (RS) fMRI revealed significant baseline differences in functional connectivity (FC) between WT and neurotransmitter-deficient mice. The fracture-induced hyperalgesia modulated central nociception and had robust impact on RS FC in all groups. The changes demonstrated in RS FC in fMRI might potentially be used as a bone traumata-induced biomarker regarding fracture healing under pathophysiological musculoskeletal conditions. The findings are of clinical importance and relevance as they advance our understanding of pain during osteoporotic fracture healing and provide a potential imaging biomarker for fracture-related hyperalgesia and its temporal development. Overall, this may help to reduce the development of chronic pain after fracture thereby improving the treatment of osteoporotic fractures. Full article

(This article belongs to the Special Issue Neurotransmitters in Neurodegenerative Diseases)

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Review

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25 pages, 2345 KiB

Open AccessReview

From Synaptic Physiology to Synaptic Pathology: The Enigma of α-Synuclein

by Kaja Nordengen and Cecilie Morland

Int. J. Mol. Sci. 2024, 25(2), 986; https://doi.org/10.3390/ijms25020986 - 12 Jan 2024

Cited by 2 | Viewed by 1161

Abstract

Alpha-synuclein (α-syn) has gained significant attention due to its involvement in neurodegenerative diseases, particularly Parkinson’s disease. However, its normal function in the human brain is equally fascinating. The α-syn protein is highly dynamic and can adapt to various conformational stages, which differ in their interaction with synaptic elements, their propensity to drive pathological aggregation, and their toxicity. This review will delve into the multifaceted role of α-syn in different types of synapses, shedding light on contributions to neurotransmission and overall brain function. We describe the physiological role of α-syn at central synapses, including the bidirectional interaction between α-syn and neurotransmitter systems. Full article

(This article belongs to the Special Issue Neurotransmitters in Neurodegenerative Diseases)

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