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State-of-the-Art Molecular Neurobiology in Italy
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State-of-the-Art Molecular Neurobiology in Italy

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 (1 December 2022) | Viewed by 18413

Special Issue Editors

Prof. Dr. Sandro Sonnino

E-Mail Website
Collection Editor
Department of Medical Biotechnology and Translational Medicine, University of Milano, 20054 Segrate, MI, Italy
Interests: gangliosides; Parkinson’s disease; mebrane organization; complex lipids; sphingosine; ceramide
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Michele Papa

E-Mail Website1 Website2
Collection Editor
Laboratory of Neuronal Networks Morphology and System Biology, Department of Mental and Physical Health and Preventive Medicine, University of Campania ‘‘Luigi Vanvitelli”, 80138 Naples, Italy
Interests: neuroinflammation; astrocytes; synaptic plasticity; nerve growth factor; vagus nerve stimulation
Special Issues, Collections and Topics in MDPI journals
Dr. Monica Bucciantini

E-Mail Website
Collection Editor
Department of Biomedical, Experimental and Clinical Sciences “Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, Italy
Interests: amyloid; cytotoxicity; inflammation; polyphenols
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Michele Maffia

E-Mail Website
Collection Editor
Department of Biological and Environmental Science and Technology, University of Salento, 73100 Lecce, Italy
Interests: cell physiology and differentiation; adaptive physiology; neurodegeneration; cancer biology; functional proteomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Topical Collection aims to provide a comprehensive overview of recent advances in molecular neurobiology in Italy by inviting contributions from Italy research institutes/laboratories that consolidate our understanding of this area. Topics include, but are not limited to, the following:

  • Neurobiology;
  • Neurochemistry;
  • Neurology;
  • Neuropathology;
  • Neurophysiology;
  • Neuropharmacology;
  • Neurogenetics;
  • Neuro oncology;
  • Aging neuroscience.

Prof. Dr. Sandro Sonnino
Prof. Dr. Michele Papa
Prof. Dr. Monica Bucciantini
Prof. Dr. Michele Maffia
Collection 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

  • neurobiology
  • neurochemistry
  • neurology
  • neuropathology
  • neurophysiology
  • neuropharmacology
  • neurogenetics
  • neuro oncology
  • aging neuroscience

Published Papers (6 papers)

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Research

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24 pages, 2067 KiB  
Article
Pharmacokinetic and Permeation Studies in Rat Brain of Natural Compounds Led to Investigate Eugenol as Direct Activator of Dopamine Release in PC12 Cells
by Barbara Pavan, Anna Bianchi, Giada Botti, Luca Ferraro, Maria Chiara Valerii, Enzo Spisni and Alessandro Dalpiaz
Int. J. Mol. Sci. 2023, 24(2), 1800; https://doi.org/10.3390/ijms24021800 - 16 Jan 2023
Cited by 6 | Viewed by 2288
Abstract
Eugenol, cinnamaldehyde and D-limonene, the main components of natural essential oils, are endowed with antioxidant and anti-inflammatory properties which allow them to induce beneficial effects on intestinal, cardiac and neuronal levels. In order to characterize their pharmacokinetic profiles and aptitude to permeate in [...] Read more.
Eugenol, cinnamaldehyde and D-limonene, the main components of natural essential oils, are endowed with antioxidant and anti-inflammatory properties which allow them to induce beneficial effects on intestinal, cardiac and neuronal levels. In order to characterize their pharmacokinetic profiles and aptitude to permeate in the central nervous system after intravenous and oral administration to rats, new analytical procedures, easily achievable with HPLC-UV techniques, were developed. The terminal half-lives of these compounds range from 12.4 ± 0.9 (D-limonene) and 23.1 ± 1.6 min (cinnamaldehyde); their oral bioavailability appears relatively poor, ranging from 4.25 ± 0.11% (eugenol) to 7.33 ± 0.37% (cinnamaldehyde). Eugenol evidences a marked aptitude to permeate in the cerebrospinal fluid (CSF) of rats following both intravenous and oral administrations, whereas cinnamaldehyde appears able to reach the CSF only after intravenous administration; limonene is totally unable to permeate in the CSF. Eugenol was therefore recruited for in vitro studies of viability and time-/dose-dependent dopamine release in neuronal differentiated PC12 cells (a recognized cellular model mimicking dopaminergic neurons), evidencing its ability to increase cell viability and to induce dopamine release according to a U-shaped time-course curve. Moreover, concentration-response data suggest that eugenol may induce beneficial effects against Parkinson’s disease after oral administration. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Italy)
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16 pages, 8100 KiB  
Article
Liver Steatosis and Steatohepatitis Alter Bile Acid Receptors in Brain and Induce Neuroinflammation: A Contribution of Circulating Bile Acids and Blood-Brain Barrier
by Noemi Fiaschini, Mariateresa Mancuso, Mirella Tanori, Eleonora Colantoni, Roberta Vitali, Gianfranco Diretto, Laura Lorenzo Rebenaque, Laura Stronati and Anna Negroni
Int. J. Mol. Sci. 2022, 23(22), 14254; https://doi.org/10.3390/ijms232214254 - 17 Nov 2022
Cited by 2 | Viewed by 2083
Abstract
A tight relationship between gut-liver diseases and brain functions has recently emerged. Bile acid (BA) receptors, bacterial-derived molecules and the blood-brain barrier (BBB) play key roles in this association. This study was aimed to evaluate how non-alcoholic fatty liver disease (NAFLD) and non-alcoholic [...] Read more.
A tight relationship between gut-liver diseases and brain functions has recently emerged. Bile acid (BA) receptors, bacterial-derived molecules and the blood-brain barrier (BBB) play key roles in this association. This study was aimed to evaluate how non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) impact the BA receptors Farnesoid X receptor (FXR) and Takeda G-protein coupled receptor 5 (TGR5) expression in the brain and to correlate these effects with circulating BAs composition, BBB integrity and neuroinflammation. A mouse model of NAFLD was set up by a high-fat and sugar diet, and NASH was induced with the supplementation of dextran-sulfate-sodium (DSS) in drinking water. FXR, TGR5 and ionized calcium-binding adaptor molecule 1 (Iba-1) expression in the brain was detected by immunohistochemistry, while Zonula occludens (ZO)-1, Occludin and Plasmalemmal Vesicle Associated Protein-1 (PV-1) were analyzed by immunofluorescence. Biochemical analyses investigated serum BA composition, lipopolysaccharide-binding protein (LBP) and S100β protein (S100β) levels. Results showed a down-regulation of FXR in NASH and an up-regulation of TGR5 and Iba-1 in the cortex and hippocampus in both treated groups as compared to the control group. The BA composition was altered in the serum of both treated groups, and LBP and S100β were significantly augmented in NASH. ZO-1 and Occludin were attenuated in the brain capillary endothelial cells of both treated groups versus the control group. We demonstrated that NAFLD and NASH provoke different grades of brain dysfunction, which are characterized by the altered expression of BA receptors, FXR and TGR5, and activation of microglia. These effects are somewhat promoted by a modification of circulating BAs composition and by an increase in LBP that concur to damage BBB, thus favoring neuroinflammation. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Italy)
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16 pages, 3760 KiB  
Article
Chronic Trazodone and Citalopram Treatments Increase Trophic Factor and Circadian Rhythm Gene Expression in Rat Brain Regions Relevant for Antidepressant Efficacy
by Lucia Carboni, Laura Rullo, Francesca Felicia Caputi, Serena Stamatakos, Sanzio Candeletti and Patrizia Romualdi
Int. J. Mol. Sci. 2022, 23(22), 14041; https://doi.org/10.3390/ijms232214041 - 14 Nov 2022
Cited by 5 | Viewed by 2033
Abstract
Trazodone is an efficacious atypical antidepressant acting both as an SSRI and a 5HT2A and 5HT2C antagonist. Antagonism to H1-histaminergic and alpha1-adrenergic receptors is responsible for a sleep-promoting action. We studied long-term gene expression modulations induced by chronic trazodone to investigate the molecular [...] Read more.
Trazodone is an efficacious atypical antidepressant acting both as an SSRI and a 5HT2A and 5HT2C antagonist. Antagonism to H1-histaminergic and alpha1-adrenergic receptors is responsible for a sleep-promoting action. We studied long-term gene expression modulations induced by chronic trazodone to investigate the molecular underpinning of trazodone efficacy. Rats received acute or chronic treatment with trazodone or citalopram. mRNA expression of growth factor and circadian rhythm genes was evaluated by qPCR in the prefrontal cortex (PFCx), hippocampus, Nucleus Accumbens (NAc), amygdala, and hypothalamus. CREB levels and phosphorylation state were evaluated using Western blotting. BDNF levels were significantly increased in PFCx and hippocampus by trazodone and in the NAc and hypothalamus by citalopram. Likewise, TrkB receptor levels augmented in the PFCx after trazodone and in the amygdala after citalopram. FGF-2 and FGFR2 levels were higher after trazodone in the PFCx. The CREB phosphorylation state was increased by chronic trazodone in the PFCx, hippocampus, and hypothalamus. Bmal1 and Per1 were increased by both antidepressants after acute and chronic treatments, while Per2 levels were specifically augmented by chronic trazodone in the PFCx and NAc, and by citalopram in the PFCx, amygdala, and NAc. These findings show that trazodone affects the expression of neurotrophic factors involved in antidepressant responses and alters circadian rhythm genes implicated in the pathophysiology of depression, thus shedding light on trazodone’s molecular mechanism of action. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Italy)
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Review

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32 pages, 1474 KiB  
Review
Autism Spectrum Disorder: Focus on Glutamatergic Neurotransmission
by Martina Montanari, Giuseppina Martella, Paola Bonsi and Maria Meringolo
Int. J. Mol. Sci. 2022, 23(7), 3861; https://doi.org/10.3390/ijms23073861 - 31 Mar 2022
Cited by 28 | Viewed by 6190
Abstract
Disturbances in the glutamatergic system have been increasingly documented in several neuropsychiatric disorders, including autism spectrum disorder (ASD). Glutamate-centered theories of ASD are based on evidence from patient samples and postmortem studies, as well as from studies documenting abnormalities in glutamatergic gene expression [...] Read more.
Disturbances in the glutamatergic system have been increasingly documented in several neuropsychiatric disorders, including autism spectrum disorder (ASD). Glutamate-centered theories of ASD are based on evidence from patient samples and postmortem studies, as well as from studies documenting abnormalities in glutamatergic gene expression and metabolic pathways, including changes in the gut microbiota glutamate metabolism in patients with ASD. In addition, preclinical studies on animal models have demonstrated glutamatergic neurotransmission deficits and altered expression of glutamate synaptic proteins. At present, there are no approved glutamatergic drugs for ASD, but several ongoing clinical trials are currently focusing on evaluating in autistic patients glutamatergic pharmaceuticals already approved for other conditions. In this review, we provide an overview of the literature concerning the role of glutamatergic neurotransmission in the pathophysiology of ASD and as a potential target for novel treatments. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Italy)
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24 pages, 1140 KiB  
Review
Pathogenetic Mechanisms of Hypertension–Brain-Induced Complications: Focus on Molecular Mediators
by Tiziana Di Chiara, Alessandro Del Cuore, Mario Daidone, Stefania Scaglione, Rosario Luca Norrito, Maria Grazia Puleo, Rosario Scaglione, Antonio Pinto and Antonino Tuttolomondo
Int. J. Mol. Sci. 2022, 23(5), 2445; https://doi.org/10.3390/ijms23052445 - 23 Feb 2022
Cited by 3 | Viewed by 3786
Abstract
There is growing evidence that hypertension is the most important vascular risk factor for the development and progression of cardiovascular and cerebrovascular diseases. The brain is an early target of hypertension-induced organ damage and may manifest as stroke, subclinical cerebrovascular abnormalities and cognitive [...] Read more.
There is growing evidence that hypertension is the most important vascular risk factor for the development and progression of cardiovascular and cerebrovascular diseases. The brain is an early target of hypertension-induced organ damage and may manifest as stroke, subclinical cerebrovascular abnormalities and cognitive decline. The pathophysiological mechanisms of these harmful effects remain to be completely clarified. Hypertension is well known to alter the structure and function of cerebral blood vessels not only through its haemodynamics effects but also for its relationships with endothelial dysfunction, oxidative stress and inflammation. In the last several years, new possible mechanisms have been suggested to recognize the molecular basis of these pathological events. Accordingly, this review summarizes the factors involved in hypertension-induced brain complications, such as haemodynamic factors, endothelial dysfunction and oxidative stress, inflammation and intervention of innate immune system, with particular regard to the role of Toll-like receptors that have to be considered dominant components of the innate immune system. The complete definition of their prognostic role in the development and progression of hypertensive brain damage will be of great help in the identification of new markers of vascular damage and the implementation of innovative targeted therapeutic strategies. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Italy)
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Other

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7 pages, 889 KiB  
Case Report
Changes in Brain Volumes Are Relevant during Natalizumab-Associated Progressive Multifocal Leukoencephalopathy: Lessons from a Case Report
by Roberto De Masi, Stefania Orlando, Silvia Armenise, Pantaleo Spagnolo, Ruggero Capra and Maria Carmela Costa
Int. J. Mol. Sci. 2022, 23(21), 13642; https://doi.org/10.3390/ijms232113642 - 07 Nov 2022
Cited by 1 | Viewed by 1245
Abstract
This is a case report concerning a Natalizumab-associated Progressive Multifocal Leukoencephalopathy (PML) with cerebellar localization and wakefulness disturbances. Awakening and clinical improvement dramatically occurred as soon as the immune reconstitution inflammatory syndrome (IRIS) took place, being it mild in nature and colocalizing with [...] Read more.
This is a case report concerning a Natalizumab-associated Progressive Multifocal Leukoencephalopathy (PML) with cerebellar localization and wakefulness disturbances. Awakening and clinical improvement dramatically occurred as soon as the immune reconstitution inflammatory syndrome (IRIS) took place, being it mild in nature and colocalizing with the PML lesion. In these ideal experimental conditions, we applied brain magnetic resonance imaging post-analysis in order to know changes in brain volumes underlying the pathological process over the infection period. White matter volume increased with a decrease in grey matter during IRIS. Conversely, we found a constant increase in cerebrospinal fluid volume throughout the duration of PML, suggesting a widespread abiotrophic effect, far from the lesion. Furthermore, brain parenchymal fraction significantly decreased as expected while the total brain volume remained stable at all times. Neurodegeneration is the main contributor to the steady disability in Natalizumab-associated PML. This process is thought to be widespread and inflammatory in nature as well as sustained by IRIS and humoral factors derived from the PML lesion. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Italy)
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