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Physiology and Pathology of Neurons 2.0
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Physiology and Pathology of Neurons 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: 30 May 2024 | Viewed by 3715

Special Issue Editor

Prof. Dr. Jacopo Meldolesi

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Guest Editor
1. San Raffaele Institute, Vita-Salute San Raffaele University, 20132 Milan, Italy
2. CNR Institute of Neuroscience, Milan-Bicocca University, 20132 Milan, Italy
Interests: neurons and their interactions with astrocytes; neurotrophin receptors; multiplicity and complexity of extracellular vesicles; non-secretory exocytosis; multiple roles of Ca2; control of gene expression; specificity of neural gene expression; neurodegenerative diseases and new therapies; synaptic pathology; astrocytes, microglia and their role in brain pathology
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Special Issue Information

Dear Colleagues,

The innovative properties of brain cells, and of neurons in particular, are continually subject to investigation by neuroscience researchers. In 2020, I contributed to these fascinating developments by governing, as the Guest Editor, a previous IJMS Special Issue (SI) entitled “Gene Expression in the Physiology and Pathology of Neurons”, which was a great success. Well-known scientists participated by contributing excellent articles and reviews in the areas of their specific competence. Upon publication and their further introduction in the general presentation of the SI, they were widely appreciated and quoted in the literature.

Based on my positive experience in the field and the ongoing development of knowledge, I propose a duplication of my first SI, as the role of neuronal genes is still a factor governing the initiation and operation of brain cells. However, the focus of this SI should also include the mechanisms and properties of relevant processes occurring in neurons, from neurogenesis to differentiation, including the acquisition, development and maintenance of their identity. Interestingly, many such processes are complex, governed by the interaction of neurons with adjacent glial cells, especially astrocytes. Other processes include various neuronal lesions and reprogramming, and their regeneration in many cases. Highly relevant to our general framework are neuronal diseases, including their therapies, which have been continuously improved by recent studies.

Based on all these considerations, I have decided to simplify the title of the duplicated SI, which is now entitled “Physiology and Pathology of Neurons”. This title includes specific processes and targets most intensely investigated by present research, for which I have represented through the 10 topics listed below. For each of these processes, a number of specialists have been identified based on their scientific articles and reviews published over the last few years. Upon accurate revision and approval, the SI contributions will be published in IJMS according to the rules of the Journal, as specified here below.

Both original research articles and comprehensive reviews are welcome, dealing with one of the following topics:

  1. Neuronal identity.
  2. Neurogenesis from astrocytes after transient ischemia.
  3. Role of miRNAs in neuronal differentiation.
  4. Neuronal repair.
  5. Axon guidance and regeneration.
  6. Development and maturation of neurons and astrocytes.
  7. Complexity of synapses.
  8. Alzheimer’s and Parkinson’s diseases, and their origin and development.
  9. Autism spectrum disorders, and the role of dendritic spines, immune mediators, astrocytes and other processes.
  10. Additional properties of neurodegenerative and other neuronal diseases.

Prof. Dr. Jacopo Meldolesi
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.

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Published Papers (3 papers)

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Research

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13 pages, 1921 KiB  
Article
Alterations in KIDINS220/ARMS Expression Impact Sensory Processing and Social Behavior in Adult Mice
by Martina Albini, Amanda Almacellas-Barbanoj, Alicja Krawczun-Rygmaczewska, Lorenzo Ciano, Fabio Benfenati, Caterina Michetti and Fabrizia Cesca
Int. J. Mol. Sci. 2024, 25(4), 2334; https://doi.org/10.3390/ijms25042334 - 16 Feb 2024
Viewed by 751
Abstract
Kinase D-interacting substrate of 220 kDa (Kidins220) is a transmembrane protein that participates in neural cell survival, maturation, and plasticity. Mutations in the human KIDINS220 gene are associated with a neurodevelopmental disorder (‘SINO’ syndrome) characterized by spastic paraplegia, intellectual disability, and in some [...] Read more.
Kinase D-interacting substrate of 220 kDa (Kidins220) is a transmembrane protein that participates in neural cell survival, maturation, and plasticity. Mutations in the human KIDINS220 gene are associated with a neurodevelopmental disorder (‘SINO’ syndrome) characterized by spastic paraplegia, intellectual disability, and in some cases, autism spectrum disorder. To better understand the pathophysiology of KIDINS220-linked pathologies, in this study, we assessed the sensory processing and social behavior of transgenic mouse lines with reduced Kidins220 expression: the CaMKII-driven conditional knockout (cKO) line, lacking Kidins220 in adult forebrain excitatory neurons, and the Kidins220floxed line, expressing constitutively lower protein levels. We show that alterations in Kidins220 expression levels and its splicing pattern cause impaired response to both auditory and olfactory stimuli. Both transgenic lines show impaired startle response to high intensity sounds, with preserved pre-pulsed inhibition, and strongly reduced social odor recognition. In the Kidins220floxed line, olfactory alterations are associated with deficits in social memory and increased aggressive behavior. Our results broaden our knowledge of the SINO syndrome; understanding sensory information processing and its deviations under neuropathological conditions is crucial for devising future therapeutic strategies to enhance the quality of life of affected individuals. Full article
(This article belongs to the Special Issue Physiology and Pathology of Neurons 2.0)
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15 pages, 7624 KiB  
Article
Peripheral Branch Injury Induces Oxytocin Receptor Expression at the Central Axon Terminals of Primary Sensory Neurons
by Heni El Heni, Péter Bátor Kemenesi-Gedei, Laura Pálvölgyi, Ivett Dorina Kozma-Szeredi and Gyöngyi Kis
Int. J. Mol. Sci. 2024, 25(1), 7; https://doi.org/10.3390/ijms25010007 - 19 Dec 2023
Viewed by 820
Abstract
Considerable evidence suggests that oxytocin, as a regulatory nonapeptide, participates in modulatory mechanisms of nociception. Nonetheless, the role of this hypothalamic hormone and its receptor in the sensory pathway has yet to be fully explored. The present study performed immunohistochemistry, enzyme-linked immunosorbent assay, [...] Read more.
Considerable evidence suggests that oxytocin, as a regulatory nonapeptide, participates in modulatory mechanisms of nociception. Nonetheless, the role of this hypothalamic hormone and its receptor in the sensory pathway has yet to be fully explored. The present study performed immunohistochemistry, enzyme-linked immunosorbent assay, and RT-qPCR analysis to assess changes in the expression of the neuronal oxytocin receptor in female rats following tight ligation of the sciatic nerve after 1, 3, and 7 days of survival. Oxytocin receptor immunoreactivity was present in both dorsal root ganglia and lumbar spinal cord segments, but not accumulated at the site of the ligation of the peripheral nerve branch. We found a time-dependent change in the expression of oxytocin receptor mRNA in L5 dorsal root ganglion neurons, as well as an increase in the level of the receptor protein in the lumbar segment of the spinal cord. A peak in the expression was observed on day 3, which downturned slightly by day 7 after the nerve ligation. These results show that OTR expression is up-regulated in response to peripheral nerve lesions. We assume that the importance of OTR is to modify spinal presynaptic inputs of the sensory neurons upon injury-induced activation, thus to be targets of the descending oxytocinergic neurons from supraspinal levels. The findings of this study support the concept that oxytocin plays a role in somatosensory transmission. Full article
(This article belongs to the Special Issue Physiology and Pathology of Neurons 2.0)
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Review

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13 pages, 10364 KiB  
Review
Autism Spectrum Disorder: Brain Areas Involved, Neurobiological Mechanisms, Diagnoses and Therapies
by Jacopo Lamanna and Jacopo Meldolesi
Int. J. Mol. Sci. 2024, 25(4), 2423; https://doi.org/10.3390/ijms25042423 - 19 Feb 2024
Viewed by 1744
Abstract
Autism spectrum disorder (ASD), affecting over 2% of the pre-school children population, includes an important fraction of the conditions accounting for the heterogeneity of autism. The disease was discovered 75 years ago, and the present review, based on critical evaluations of the recognized [...] Read more.
Autism spectrum disorder (ASD), affecting over 2% of the pre-school children population, includes an important fraction of the conditions accounting for the heterogeneity of autism. The disease was discovered 75 years ago, and the present review, based on critical evaluations of the recognized ASD studies from the beginning of 1990, has been further developed by the comparative analyses of the research and clinical reports, which have grown progressively in recent years up to late 2023. The tools necessary for the identification of the ASD disease and its related clinical pathologies are genetic and epigenetic mutations affected by the specific interaction with transcription factors and chromatin remodeling processes occurring within specific complexes of brain neurons. Most often, the ensuing effects induce the inhibition/excitation of synaptic structures sustained primarily, at dendritic fibers, by alterations of flat and spine response sites. These effects are relevant because synapses, established by specific interactions of neurons with glial cells, operate as early and key targets of ASD. The pathology of children is often suspected by parents and communities and then confirmed by ensuing experiences. The final diagnoses of children and mature patients are then completed by the combination of neuropsychological (cognitive) tests and electro-/magneto-encephalography studies developed in specialized centers. ASD comorbidities, induced by processes such as anxieties, depressions, hyperactivities, and sleep defects, interact with and reinforce other brain diseases, especially schizophrenia. Advanced therapies, prescribed to children and adult patients for the control of ASD symptoms and disease, are based on the combination of well-known brain drugs with classical tools of neurologic and psychiatric practice. Overall, this review reports and discusses the advanced knowledge about the biological and medical properties of ASD. Full article
(This article belongs to the Special Issue Physiology and Pathology of Neurons 2.0)
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