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Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding...
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Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (1 October 2021) | Viewed by 31090

Special Issue Editors

Dr. Cristina Fasolato

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padua, Via U. Bassi 58/B, 35131 Padua, Italy
Interests: Ca2+ imaging; electrophysiology; neurobiology; neurodegeneration; Alzheimer’s disease; presenilins; amyloid-beta; brain oscillations
Dr. Elisa Greotti

E-Mail Website
Guest Editor
1. Department of Biomedical Sciences, University of Padua, 35131 Padua, Italy
2. Neuroscience Institute, National Research Council (CNR), 35131 Padua, Italy
Interests: Ca2+ imaging; genetically-encoded Ca2+ sensors; mitochondria; optogenetics; neurodegeneration; Alzheimer's disease
Dr. Alessandro Leparulo

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padua, 35131 Padua, Italy
Interests: electrophysiology; connexins; brain oscillations; local field potentials; Alzheimer’s disease; neurophysiology; neurodegeneration

Special Issue Information

Dear Colleagues,

The prevalence of brain disorders and neurodegenerative diseases has significantly increased, but effective therapies are still lacking for most of them. Whether brain aging shares similarities with the neurodegenerative process is not yet clear. Some brain disorders, which differ in terms of origin and clinical development, can share common characteristics, particularly in their early stages. Dysregulation of cell signalling eventually leads to excitatory/inhibitory neuronal imbalance, which is often associated with undetected epileptic seizures. A better understanding of intra- and intercellular signalling between the different types of cells of the central nervous system and the development of tools to investigate cellular pathways and brain networks could lead to new insights useful for the study of the healthy and sick brain.

The aim of this Special Issue is to extend our horizons, shed light on neglected pathways and actors, and test dogmas in the field of aging and neurodegenerative diseases, possibly offering new strategies to maintain brain function and fight neurodegeneration.

Dr. Cristina Fasolato
Dr. Elisa Greotti
Dr. Alessandro Leparulo
Guest Editors

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Keywords

  • aging
  • neurodegeneration
  • brain tumors
  • stroke
  • neurons
  • astrocytes
  • microglia
  • oligodendrocytes
  • pericytes
  • cell signalling
  • animal models
  • brain circuits

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Published Papers (7 papers)

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Research

Jump to: Review

24 pages, 11834 KiB  
Article
Astrocytes Modulate Somatostatin Interneuron Signaling in the Visual Cortex
by Vanessa Jorge Henriques, Angela Chiavegato, Giorgio Carmignoto and Marta Gómez-Gonzalo
Cells 2022, 11(9), 1400; https://doi.org/10.3390/cells11091400 - 20 Apr 2022
Cited by 5 | Viewed by 3712
Abstract
At glutamatergic synapses, astrocytes respond to the neurotransmitter glutamate with intracellular Ca2+ elevations and the release of gliotransmitters that modulate synaptic transmission. While the functional interactions between neurons and astrocytes have been intensively studied at glutamatergic synapses, the role of astrocytes at [...] Read more.
At glutamatergic synapses, astrocytes respond to the neurotransmitter glutamate with intracellular Ca2+ elevations and the release of gliotransmitters that modulate synaptic transmission. While the functional interactions between neurons and astrocytes have been intensively studied at glutamatergic synapses, the role of astrocytes at GABAergic synapses has been less investigated. In the present study, we combine optogenetics with 2-photon Ca2+ imaging experiments and patch-clamp recording techniques to investigate the signaling between Somatostatin (SST)-releasing GABAergic interneurons and astrocytes in brain slice preparations from the visual cortex (VCx). We found that an intense stimulation of SST interneurons evokes Ca2+ elevations in astrocytes that fundamentally depend on GABAB receptor (GABABR) activation, and that this astrocyte response is modulated by the neuropeptide somatostatin. After episodes of SST interneuron hyperactivity, we also observed a long-lasting reduction of the inhibitory postsynaptic current (IPSC) amplitude onto pyramidal neurons (PNs). This reduction of inhibitory tone (i.e., disinhibition) is counterbalanced by the activation of astrocytes that upregulate SST interneuron-evoked IPSC amplitude by releasing ATP that, after conversion to adenosine, activates A1Rs. Our results describe a hitherto unidentified modulatory mechanism of inhibitory transmission to VCx layer II/III PNs that involves the functional recruitment of astrocytes by SST interneuron signaling. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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21 pages, 6193 KiB  
Article
Accelerated Aging Characterizes the Early Stage of Alzheimer’s Disease
by Alessandro Leparulo, Marta Bisio, Nelly Redolfi, Tullio Pozzan, Stefano Vassanelli and Cristina Fasolato
Cells 2022, 11(2), 238; https://doi.org/10.3390/cells11020238 - 11 Jan 2022
Cited by 11 | Viewed by 2508
Abstract
For Alzheimer’s disease (AD), aging is the main risk factor, but whether cognitive impairments due to aging resemble early AD deficits is not yet defined. When working with mouse models of AD, the situation is just as complicated, because only a few studies [...] Read more.
For Alzheimer’s disease (AD), aging is the main risk factor, but whether cognitive impairments due to aging resemble early AD deficits is not yet defined. When working with mouse models of AD, the situation is just as complicated, because only a few studies track the progression of the disease at different ages, and most ignore how the aging process affects control mice. In this work, we addressed this problem by comparing the aging process of PS2APP (AD) and wild-type (WT) mice at the level of spontaneous brain electrical activity under anesthesia. Using local field potential recordings, obtained with a linear probe that traverses the posterior parietal cortex and the entire hippocampus, we analyzed how multiple electrical parameters are modified by aging in AD and WT mice. With this approach, we highlighted AD specific features that appear in young AD mice prior to plaque deposition or that are delayed at 12 and 16 months of age. Furthermore, we identified aging characteristics present in WT mice but also occurring prematurely in young AD mice. In short, we found that reduction in the relative power of slow oscillations (SO) and Low/High power imbalance are linked to an AD phenotype at its onset. The loss of SO connectivity and cortico-hippocampal coupling between SO and higher frequencies as well as the increase in UP-state and burst durations are found in young AD and old WT mice. We show evidence that the aging process is accelerated by the mutant PS2 itself and discuss such changes in relation to amyloidosis and gliosis. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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20 pages, 5916 KiB  
Article
Aberrant Patterns of Sensory-Evoked Activity in the Olfactory Bulb of LRRK2 Knockout Mice
by Andrea Maset, Marco Albanesi, Antonio di Soccio, Martina Canova, Marco dal Maschio and Claudia Lodovichi
Cells 2021, 10(11), 3212; https://doi.org/10.3390/cells10113212 - 17 Nov 2021
Cited by 4 | Viewed by 2672
Abstract
The LRRK2 gene is the major genetic determinant of familiar Parkinson’s disease (PD). Leucine-rich repeat kinase 2 (LRRK2) is a multidomain protein involved in several intracellular signaling pathways. A wealth of evidence indicates that LRRK2 is enriched at the presynaptic compartment where it [...] Read more.
The LRRK2 gene is the major genetic determinant of familiar Parkinson’s disease (PD). Leucine-rich repeat kinase 2 (LRRK2) is a multidomain protein involved in several intracellular signaling pathways. A wealth of evidence indicates that LRRK2 is enriched at the presynaptic compartment where it regulates vesicle trafficking and neurotransmitter release. However, whether the role of LRRK2 affects neuronal networks dynamic at systems level remains unknown. Addressing this question is critical to unravel the impact of LRRK2 on brain function. Here, combining behavioral tests, electrophysiological recordings, and functional imaging, we investigated neuronal network dynamics, in vivo, in the olfactory bulb of mice carrying a null mutation in LRRK2 gene (LRRK2 knockout, LRRK2 KO, mice). We found that LRRK2 KO mice exhibit olfactory behavioral deficits. At the circuit level, the lack of LRRK2 expression results in altered gamma rhythms and odorant-evoked activity with significant impairments, while the spontaneous activity exhibited limited alterations. Overall, our data in the olfactory bulb suggest that the multifaced role of LRRK2 has a strong impact at system level when the network is engaged in active sensory processing. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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Review

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39 pages, 2039 KiB  
Review
Optogenetic Methods to Investigate Brain Alterations in Preclinical Models
by Marco Brondi, Matteo Bruzzone, Claudia Lodovichi and Marco dal Maschio
Cells 2022, 11(11), 1848; https://doi.org/10.3390/cells11111848 - 5 Jun 2022
Cited by 6 | Viewed by 3640
Abstract
Investigating the neuronal dynamics supporting brain functions and understanding how the alterations in these mechanisms result in pathological conditions represents a fundamental challenge. Preclinical research on model organisms allows for a multiscale and multiparametric analysis in vivo of the neuronal mechanisms and holds [...] Read more.
Investigating the neuronal dynamics supporting brain functions and understanding how the alterations in these mechanisms result in pathological conditions represents a fundamental challenge. Preclinical research on model organisms allows for a multiscale and multiparametric analysis in vivo of the neuronal mechanisms and holds the potential for better linking the symptoms of a neurological disorder to the underlying cellular and circuit alterations, eventually leading to the identification of therapeutic/rescue strategies. In recent years, brain research in model organisms has taken advantage, along with other techniques, of the development and continuous refinement of methods that use light and optical approaches to reconstruct the activity of brain circuits at the cellular and system levels, and to probe the impact of the different neuronal components in the observed dynamics. These tools, combining low-invasiveness of optical approaches with the power of genetic engineering, are currently revolutionizing the way, the scale and the perspective of investigating brain diseases. The aim of this review is to describe how brain functions can be investigated with optical approaches currently available and to illustrate how these techniques have been adopted to study pathological alterations of brain physiology. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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19 pages, 33449 KiB  
Review
Translational Stroke Research Review: Using the Mouse to Model Human Futile Recanalization and Reperfusion Injury in Ischemic Brain Tissue
by Emilia Conti, Benedetta Piccardi, Alessandro Sodero, Laura Tudisco, Ivano Lombardo, Enrico Fainardi, Patrizia Nencini, Cristina Sarti, Anna Letizia Allegra Mascaro and Marzia Baldereschi
Cells 2021, 10(12), 3308; https://doi.org/10.3390/cells10123308 - 25 Nov 2021
Cited by 9 | Viewed by 4343
Abstract
The approach to reperfusion therapies in stroke patients is rapidly evolving, but there is still no explanation why a substantial proportion of patients have a poor clinical prognosis despite successful flow restoration. This issue of futile recanalization is explained here by three clinical [...] Read more.
The approach to reperfusion therapies in stroke patients is rapidly evolving, but there is still no explanation why a substantial proportion of patients have a poor clinical prognosis despite successful flow restoration. This issue of futile recanalization is explained here by three clinical cases, which, despite complete recanalization, have very different outcomes. Preclinical research is particularly suited to characterize the highly dynamic changes in acute ischemic stroke and identify potential treatment targets useful for clinical translation. This review surveys the efforts taken so far to achieve mouse models capable of investigating the neurovascular underpinnings of futile recanalization. We highlight the translational potential of targeting tissue reperfusion in fully recanalized mouse models and of investigating the underlying pathophysiological mechanisms from subcellular to tissue scale. We suggest that stroke preclinical research should increasingly drive forward a continuous and circular dialogue with clinical research. When the preclinical and the clinical stroke research are consistent, translational success will follow. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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19 pages, 809 KiB  
Review
Cell-to-Cell Interactions Mediating Functional Recovery after Stroke
by Claudia Alia, Daniele Cangi, Verediana Massa, Marco Salluzzo, Livia Vignozzi, Matteo Caleo and Cristina Spalletti
Cells 2021, 10(11), 3050; https://doi.org/10.3390/cells10113050 - 6 Nov 2021
Cited by 10 | Viewed by 4759
Abstract
Ischemic damage in brain tissue triggers a cascade of molecular and structural plastic changes, thus influencing a wide range of cell-to-cell interactions. Understanding and manipulating this scenario of intercellular connections is the Holy Grail for post-stroke neurorehabilitation. Here, we discuss the main findings [...] Read more.
Ischemic damage in brain tissue triggers a cascade of molecular and structural plastic changes, thus influencing a wide range of cell-to-cell interactions. Understanding and manipulating this scenario of intercellular connections is the Holy Grail for post-stroke neurorehabilitation. Here, we discuss the main findings in the literature related to post-stroke alterations in cell-to-cell interactions, which may be either detrimental or supportive for functional recovery. We consider both neural and non-neural cells, starting from astrocytes and reactive astrogliosis and moving to the roles of the oligodendrocytes in the support of vulnerable neurons and sprouting inhibition. We discuss the controversial role of microglia in neural inflammation after injury and we conclude with the description of post-stroke alterations in pyramidal and GABAergic cells interactions. For all of these sections, we review not only the spontaneous evolution in cellular interactions after ischemic injury, but also the experimental strategies which have targeted these interactions and that are inspiring novel therapeutic strategies for clinical application. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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24 pages, 2624 KiB  
Review
ATM Protein Kinase: Old and New Implications in Neuronal Pathways and Brain Circuitry
by Lara Pizzamiglio, Elisa Focchi and Flavia Antonucci
Cells 2020, 9(9), 1969; https://doi.org/10.3390/cells9091969 - 26 Aug 2020
Cited by 19 | Viewed by 8462
Abstract
Despite that the human autosomal recessive disease ataxia telangiectasia (A-T) is a rare pathology, interest in the function of ataxia-telangiectasia mutated protein (ATM) is extensive. From a clinical point of view, the role of ATM in the central nervous system (CNS) is the [...] Read more.
Despite that the human autosomal recessive disease ataxia telangiectasia (A-T) is a rare pathology, interest in the function of ataxia-telangiectasia mutated protein (ATM) is extensive. From a clinical point of view, the role of ATM in the central nervous system (CNS) is the most impacting, as motor disability is the predominant symptom affecting A-T patients. Coherently, spino-cerebellar neurodegeneration is the principal hallmark of A-T and other CNS regions such as dentate and olivary nuclei and brain stem are implicated in A-T pathophysiology. Recently, several preclinical studies also highlighted the involvement of ATM in the cerebral cortex and hippocampus, thus extending A-T symptomatology to new brain areas and pathways. Here, we review old and recent evidence that largely demonstrates not only the historical ATM account in DNA damage response and cell cycle regulation, but the multiple pathways through which ATM controls oxidative stress homeostasis, insulin signalling pathways, epigenetic regulation, synaptic transmission, and excitatory–inhibitory balance. We also summarise recent evidence on ATM implication in neurological and cognitive diseases beyond A-T, bringing out ATM as new pathological substrate and potential therapeutic target. Full article
(This article belongs to the Special Issue Intra- and Intercellular Signalling in Healthy and Diseased Brain: Shedding Light on Emerging Cellular Pathways and Brain Circuits)
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