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Recent Molecular Research of Neuroscience: Application of Animal Models
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Recent Molecular Research of Neuroscience: Application of Animal Models

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: 20 January 2025 | Viewed by 4522

Special Issue Editors

Dr. Alon Lai

E-Mail Website
Guest Editor
Iatridis Spine Bioengineering Laboratory, Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: spine; back pain and intervertebral disc degeneration
Dr. Ana Chee

E-Mail Website
Guest Editor
Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA
Interests: biological repair and regeneration of the intervertebral disc; Anti-inflammatory therapies for discogenic back pain; Cell therapies for disc degenerative disease and associated disorders; Peripherally restricted non-addictive opioid treatments for chronic back pain

Special Issue Information

Dear Colleagues,

The realm of molecular neuroscience stands at the forefront of scientific inquiry, offering profound insights into the enigmatic operations of the central and peripheral nervous systems, including the brain, spinal cord, dorsal root ganglion, peripheral nerves, neurons and neurotransmitters. On the molecular level, decades of neuroscience research has provided a better understanding of the intricate workings of the complex nervous system revealing both normal and pathological functions. Advances gained from this field have wide-ranging applications such as developing treatments for neurological disorders, improving education strategies, and enhancing mental health interventions.

A significant facet of contemporary molecular neuroscience research lies in the strategic utilization of animal models, which serve as indispensable tools for investigating the complexities of neural mechanisms at the molecular level, as well as the relationship between behavioral changes and pathology-associated neurological remodeling.

Here, we invite investigators to contribute original research and review articles on the landscape of neuroscience, focusing specifically on the integral role of animal models in advancing our comprehension of the molecular mechanisms of the nervous system, identifying those associated with different pathological conditions, and translating these findings into breakthrough novel therapeutic strategies for addressing a myriad of neurological disorders.

Dr. Alon Lai
Dr. Ana V. Chee
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.

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Published Papers (4 papers)

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Research

19 pages, 3051 KiB  
Article
Cerebellar Metabolic Connectivity during Treadmill Walking before and after Unilateral Dopamine Depletion in Rats
by Heike Endepols, Nadine Apetz, Lukas Vieth, Christoph Lesser, Léon Schulte-Holtey, Bernd Neumaier and Alexander Drzezga
Int. J. Mol. Sci. 2024, 25(16), 8617; https://doi.org/10.3390/ijms25168617 - 7 Aug 2024
Viewed by 360
Abstract
Compensatory changes in brain connectivity keep motor symptoms mild in prodromal Parkinson’s disease. Studying compensation in patients is hampered by the steady progression of the disease and a lack of individual baseline controls. Furthermore, combining fMRI with walking is intricate. We therefore used [...] Read more.
Compensatory changes in brain connectivity keep motor symptoms mild in prodromal Parkinson’s disease. Studying compensation in patients is hampered by the steady progression of the disease and a lack of individual baseline controls. Furthermore, combining fMRI with walking is intricate. We therefore used a seed-based metabolic connectivity analysis based on 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) uptake in a unilateral 6-OHDA rat model. At baseline and in the chronic phase 6–7 months after lesion, rats received an intraperitoneal injection of [18F]FDG and spent 50 min walking on a horizontal treadmill, followed by a brain PET-scan under anesthesia. High activity was found in the cerebellar anterior vermis in both conditions. At baseline, the anterior vermis showed hardly any stable connections to the rest of the brain. The (future) ipsilesional cerebellar hemisphere was not particularly active during walking but was extensively connected to many brain areas. After unilateral dopamine depletion, rats still walked normally without obvious impairments. The ipsilesional cerebellar hemisphere increased its activity, but narrowed its connections down to the vestibulocerebellum, probably aiding lateral stability. The anterior vermis established a network involving the motor cortex, hippocampus and thalamus. Adding those regions to the vermis network of (previously) automatic control of locomotion suggests that after unilateral dopamine depletion considerable conscious and cognitive effort has to be provided to achieve stable walking. Full article
(This article belongs to the Special Issue Recent Molecular Research of Neuroscience: Application of Animal Models)
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16 pages, 4965 KiB  
Article
Severe Hypothermia Induces Ferroptosis in Cerebral Cortical Nerve Cells
by Chao-Long Lu, Jing-Jing Sha, Ru-Fei Ma, Xue-Tong Dong, Xiao-Rui Su, Bin Cong and Song-Jun Wang
Int. J. Mol. Sci. 2024, 25(15), 8086; https://doi.org/10.3390/ijms25158086 - 25 Jul 2024
Viewed by 361
Abstract
Abnormal shifts in global climate, leading to extreme weather, significantly threaten the safety of individuals involved in outdoor activities. Hypothermia-induced coma or death frequently occurs in clinical and forensic settings. Despite this, the precise mechanism of central nervous system injury due to hypothermia [...] Read more.
Abnormal shifts in global climate, leading to extreme weather, significantly threaten the safety of individuals involved in outdoor activities. Hypothermia-induced coma or death frequently occurs in clinical and forensic settings. Despite this, the precise mechanism of central nervous system injury due to hypothermia remains unclear, hindering the development of targeted clinical treatments and specific forensic diagnostic indicators. The GEO database was searched to identify datasets related to hypothermia. Post-bioinformatics analyses, DEGs, and ferroptosis-related DEGs (FerrDEGs) were intersected. GSEA was then conducted to elucidate the functions of the Ferr-related genes. Animal experiments conducted in this study demonstrated that hypothermia, compared to the control treatment, can induce significant alterations in iron death-related genes such as PPARG, SCD, ADIPOQ, SAT1, EGR1, and HMOX1 in cerebral cortex nerve cells. These changes lead to iron ion accumulation, lipid peroxidation, and marked expression of iron death-related proteins. The application of the iron death inhibitor Ferrostatin-1 (Fer-1) effectively modulates the expression of these genes, reduces lipid peroxidation, and improves the expression of iron death-related proteins. Severe hypothermia disrupts the metabolism of cerebral cortex nerve cells, causing significant alterations in ferroptosis-related genes. These genetic changes promote ferroptosis through multiple pathways. Full article
(This article belongs to the Special Issue Recent Molecular Research of Neuroscience: Application of Animal Models)
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16 pages, 2186 KiB  
Article
Comparison of the Influence of Bisphenol A and Bisphenol S on the Enteric Nervous System of the Mouse Jejunum
by Krystyna Makowska and Sławomir Gonkowski
Int. J. Mol. Sci. 2024, 25(13), 6941; https://doi.org/10.3390/ijms25136941 - 25 Jun 2024
Viewed by 791
Abstract
Bisphenols are dangerous endocrine disruptors that pollute the environment. Due to their chemical properties, they are globally used to produce plastics. Structural similarities to oestrogen allow bisphenols to bind to oestrogen receptors and affect internal body systems. Most commonly used in the plastic [...] Read more.
Bisphenols are dangerous endocrine disruptors that pollute the environment. Due to their chemical properties, they are globally used to produce plastics. Structural similarities to oestrogen allow bisphenols to bind to oestrogen receptors and affect internal body systems. Most commonly used in the plastic industry is bisphenol A (BPA), which also has negative effects on the nervous, immune, endocrine, and cardiovascular systems. A popular analogue of BPA-bisphenol S (BPS) also seems to have harmful effects similar to BPA on living organisms. Therefore, with the use of double immunofluorescence labelling, this study aimed to compare the effect of BPA and BPS on the enteric nervous system (ENS) in mouse jejunum. The study showed that both studied toxins impact the number of nerve cells immunoreactive to substance P (SP), galanin (GAL), vasoactive intestinal polypeptide (VIP), the neuronal isoform of nitric oxide synthase (nNOS), and vesicular acetylcholine transporter (VAChT). The observed changes were similar in the case of both tested bisphenols. However, the influence of BPA showed stronger changes in neurochemical coding. The results also showed that long-term exposure to BPS significantly affects the ENS. Full article
(This article belongs to the Special Issue Recent Molecular Research of Neuroscience: Application of Animal Models)
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23 pages, 7834 KiB  
Article
Annulus Fibrosus Injury Induces Acute Neuroinflammation and Chronic Glial Response in Dorsal Root Ganglion and Spinal Cord—An In Vivo Rat Discogenic Pain Model
by Alon Lai, Denise Iliff, Kashaf Zaheer, Jennifer Gansau, Damien M. Laudier, Venetia Zachariou and James C. Iatridis
Int. J. Mol. Sci. 2024, 25(3), 1762; https://doi.org/10.3390/ijms25031762 - 1 Feb 2024
Viewed by 2155
Abstract
Chronic painful intervertebral disc (IVD) degeneration (i.e., discogenic pain) is a major source of global disability needing improved knowledge on multiple-tissue interactions and how they progress in order improve treatment strategies. This study used an in vivo rat annulus fibrosus (AF) injury-driven discogenic [...] Read more.
Chronic painful intervertebral disc (IVD) degeneration (i.e., discogenic pain) is a major source of global disability needing improved knowledge on multiple-tissue interactions and how they progress in order improve treatment strategies. This study used an in vivo rat annulus fibrosus (AF) injury-driven discogenic pain model to investigate the acute and chronic changes in IVD degeneration and spinal inflammation, as well as sensitization, inflammation, and remodeling in dorsal root ganglion (DRG) and spinal cord (SC) dorsal horn. AF injury induced moderate IVD degeneration with acute and broad spinal inflammation that progressed to DRG to SC changes within days and weeks, respectively. Specifically, AF injury elevated macrophages in the spine (CD68) and DRGs (Iba1) that peaked at 3 days post-injury, and increased microglia (Iba1) in SC that peaked at 2 weeks post-injury. AF injury also triggered glial responses with elevated GFAP in DRGs and SC at least 8 weeks post-injury. Spinal CD68 and SC neuropeptide Substance P both remained elevated at 8 weeks, suggesting that slow and incomplete IVD healing provides a chronic source of inflammation with continued SC sensitization. We conclude that AF injury-driven IVD degeneration induces acute spinal, DRG, and SC inflammatory crosstalk with sustained glial responses in both DRGs and SC, leading to chronic SC sensitization and neural plasticity. The known association of these markers with neuropathic pain suggests that therapeutic strategies for discogenic pain need to target both spinal and nervous systems, with early strategies managing acute inflammatory processes, and late strategies targeting chronic IVD inflammation, SC sensitization, and remodeling. Full article
(This article belongs to the Special Issue Recent Molecular Research of Neuroscience: Application of Animal Models)
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