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The Role of Norepinephrine in Neuroprotection
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The Role of Norepinephrine in Neuroprotection

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (1 October 2021) | Viewed by 5367

Special Issue Editors

Prof. Dr. Francesco Fornai

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Guest Editor
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56124 Pisa, Italy
Interests: neuroanatomy; neuroscience; neurodegeneration; methamphetamine; autophagy; movement disorders; substances of abuse; morphology; ultrastructure
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Filippo Sean Giorgi

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Guest Editor
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy
Interests: noradrenaline; neurodegeneration; epilepsy

Special Issue Information

Dear Colleagues,

I am pleased to announce this Special Issue entitled “The Role of Norepinephrine in Neuroprotection”.

Most of brain norepinephrine (NE) is produced by neurons belonging to the locus coeruleus (LC), which send their efferents to the whole cortical mantle and to several subcortical structures. LC is degenerated early and significantly in several neurodegenerative disorders, and especially in Parkinson’s and Alzheimer’s disease. Thus, NE released by LC may play a critical role in the physiopathology of the neuronal degeneration occurring in these diseases. Several studies in the last few decades have shown a neuroprotective effect of NE on the neuronal damage induced by different neurotoxins. This has been evaluated by several authors in vivo, after administration in different animal species of the neurotoxins specific to dopaminergic nigrostriatal neurons and, more recently, also in vitro. Old studies proposed a key role of the release of growth factors on the neuroprotective effects of NE, whilst more recent studies are disclosing further potential mechanisms.

For instance, these are evidenced by (i) the modulation of neuroinflammation by NE through a direct effect on microglial cells and astrocytes; (ii) an effect of NE on the cellular mechanisms involved in neuroprotection. Disclosing the mechanisms by which NE from LC, as well as less explored NE nuclei of the brainstem, potentially exerts neuroprotection might reveal innovative disease-modifying therapeutic approaches. In the present Special Issue, original research contributions and focused reviews will address in detail innovative or consolidated experimental settings in which the neuroprotective effect of NE can be tested, either in vivo or in vitro, as well as the potential molecular cellular mechanisms through which this might occur.

Prof. Dr. Francesco Fornai
Prof. Dr. Filippo Sean Giorgi
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

Locus coeruleus; Brainstem norepinephrine nuclei; Degenerative disorders; Neuroprotecion; Epilepsy; Parkinson’s disease; Alzheimer’s disease; Drug abuse

Published Papers (2 papers)

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Research

17 pages, 2884 KiB  
Article
Pain Modulation from the Locus Coeruleus in a Model of Hydrocephalus: Searching for Oxidative Stress-Induced Noradrenergic Neuroprotection
by Marta Louçano, Joana Oliveira, Isabel Martins, Rui Vaz and Isaura Tavares
Int. J. Mol. Sci. 2022, 23(7), 3970; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073970 - 02 Apr 2022
Cited by 1 | Viewed by 1987
Abstract
Pain transmission at the spinal cord is modulated by noradrenaline (NA)-mediated actions that arise from supraspinal areas. We studied the locus coeruleus (LC) to evaluate the expression of the cathecolamine-synthetizing enzyme tyrosine hydroxylase (TH) and search for local oxidative stress and possible consequences [...] Read more.
Pain transmission at the spinal cord is modulated by noradrenaline (NA)-mediated actions that arise from supraspinal areas. We studied the locus coeruleus (LC) to evaluate the expression of the cathecolamine-synthetizing enzyme tyrosine hydroxylase (TH) and search for local oxidative stress and possible consequences in descending pain modulation in a model of hydrocephalus, a disease characterized by enlargement of the cerebral ventricular system usually due to the obstruction of cerebrospinal fluid flow. Four weeks after kaolin injection into the cisterna magna, immunodetection of the catecholamine-synthetizing enzymes TH and dopamine-β-hydroxylase (DBH) was performed in the LC and spinal cord. Colocalization of the oxidative stress marker 8-OHdG (8-hydroxyguanosine; 8-OHdG), with TH in the LC was performed. Formalin was injected in the hindpaw both for behavioral nociceptive evaluation and the immunodetection of Fos expression in the spinal cord. Hydrocephalic rats presented with a higher expression of TH at the LC, of TH and DBH at the spinal dorsal horn along with decreased nociceptive behavioral responses in the second (inflammatory) phase of the formalin test, and formalin-evoked Fos expression at the spinal dorsal horn. The expression of 8-OHdG was increased in the LC neurons, with higher co-localization in TH-immunoreactive neurons. Collectively, the results indicate increased noradrenergic expression at the LC during hydrocephalus. The strong oxidative stress damage at the LC neurons may lead to local neuroprotective-mediated increases in NA levels. The increased expression of catecholamine-synthetizing enzymes along with the decreased nociception-induced neuronal activation of dorsal horn neurons and behavioral pain signs may indicate that hydrocephalus is associated with alterations in descending pain modulation. Full article
(This article belongs to the Special Issue The Role of Norepinephrine in Neuroprotection)
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34 pages, 16575 KiB  
Article
Norepinephrine Protects against Methamphetamine Toxicity through β2-Adrenergic Receptors Promoting LC3 Compartmentalization
by Gloria Lazzeri, Carla L. Busceti, Francesca Biagioni, Cinzia Fabrizi, Gabriele Morucci, Filippo S. Giorgi, Michela Ferrucci, Paola Lenzi, Stefano Puglisi-Allegra and Francesco Fornai
Int. J. Mol. Sci. 2021, 22(13), 7232; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22137232 - 05 Jul 2021
Cited by 9 | Viewed by 2729
Abstract
Norepinephrine (NE) neurons and extracellular NE exert some protective effects against a variety of insults, including methamphetamine (Meth)-induced cell damage. The intimate mechanism of protection remains difficult to be analyzed in vivo. In fact, this may occur directly on target neurons or as [...] Read more.
Norepinephrine (NE) neurons and extracellular NE exert some protective effects against a variety of insults, including methamphetamine (Meth)-induced cell damage. The intimate mechanism of protection remains difficult to be analyzed in vivo. In fact, this may occur directly on target neurons or as the indirect consequence of NE-induced alterations in the activity of trans-synaptic loops. Therefore, to elude neuronal networks, which may contribute to these effects in vivo, the present study investigates whether NE still protects when directly applied to Meth-treated PC12 cells. Meth was selected based on its detrimental effects along various specific brain areas. The study shows that NE directly protects in vitro against Meth-induced cell damage. The present study indicates that such an effect fully depends on the activation of plasma membrane β2-adrenergic receptors (ARs). Evidence indicates that β2-ARs activation restores autophagy, which is impaired by Meth administration. This occurs via restoration of the autophagy flux and, as assessed by ultrastructural morphometry, by preventing the dissipation of microtubule-associated protein 1 light chain 3 (LC3) from autophagy vacuoles to the cytosol, which is produced instead during Meth toxicity. These findings may have an impact in a variety of degenerative conditions characterized by NE deficiency along with autophagy impairment. Full article
(This article belongs to the Special Issue The Role of Norepinephrine in Neuroprotection)
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