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  1. Book: Immunocytochemistry and related techniques

    Merighi, Adalberto / Lossi, Laura

    (Neuromethods, ; 101 ; Springer protocols)

    2015  

    Author's details ed. by Adalberto Merighi and Laura Lossi
    Series title Neuromethods, ; 101
    Springer protocols
    Neuromethods
    Collection Neuromethods
    Keywords Immunohistochemistry / methods ; Histocytological Preparation Techniques / methods ; Cell Physiological Processes ; Chemistry Techniques, Analytical / methods
    Language English
    Size XIII, 473 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT018749798
    ISBN 978-1-4939-2312-0 ; 9781493923137 ; 1-4939-2312-9 ; 1493923137
    Database Catalogue ZB MED Medicine, Health

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  2. Book: Neuronal cell death

    Lossi, Laura / Merighi, Adalberto

    methods and protocols

    (Methods in molecular biology ; 1254 ; Springer protocols)

    2015  

    Author's details ed. by Laura Lossi and Adalberto Merighi
    Series title Methods in molecular biology ; 1254
    Springer protocols
    Collection
    Keywords Cell death ; Nervous system/Degeneration ; Neurons
    Subject code 571.936
    Language English
    Size XIV, 396 S. : Ill., graph. Darst., 27 cm
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT018512202
    ISBN 978-1-4939-2151-5 ; 9781493921522 ; 1-4939-2151-7 ; 1493921525
    Database Catalogue ZB MED Medicine, Health

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  3. Book: Neuropeptides

    Merighi, Adalberto

    methods and protocols

    (Methods in molecular biology ; 789 ; Springer protocols)

    2011  

    Author's details ed. by Adalberto Merighi
    Series title Methods in molecular biology ; 789
    Springer protocols
    Collection
    Language English
    Size 350 S.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT016889674
    ISBN 978-1-61779-309-7 ; 9781617793103 ; 1-61779-309-4 ; 1617793108
    Database Catalogue ZB MED Medicine, Health

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  4. Article: Cross Talk of BDNF and GDNF in Spinal Substantia Gelatinosa (Lamina II): Focus on Circuitry.

    Merighi, Adalberto

    Advances in experimental medicine and biology

    2021  Volume 1331, Page(s) 215–229

    Abstract: BDNF and GDNF display the notable qualities of undergoing a regulated secretion in neurons and being anterogradely transported to nerve terminals, where they can modulate fast synaptic transmission. That BDNF positively modulates nociception and/or pain ... ...

    Abstract BDNF and GDNF display the notable qualities of undergoing a regulated secretion in neurons and being anterogradely transported to nerve terminals, where they can modulate fast synaptic transmission. That BDNF positively modulates nociception and/or pain is today widely accepted, as the growth factor can start and maintain physiological and pathological pain. The contribution of GDNF to nociception is by far most elusive, but evidence is accumulating that the molecule displays analgesic activity, at least in rodents. Here I resume the current knowledge on the spinal cord circuits in which these two factors may act as modulators of pain-related synaptic transmission, focusing on their structural and functional interplay in the regulation of nociception and pain.
    MeSH term(s) Brain-Derived Neurotrophic Factor/genetics ; Glial Cell Line-Derived Neurotrophic Factor/genetics ; Neurons ; Spinal Cord ; Substantia Gelatinosa ; Synaptic Transmission
    Chemical Substances Brain-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor
    Language English
    Publishing date 2021-08-28
    Publishing country United States
    Document type Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-3-030-74046-7_14
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book ; Online: Reelin-Related Neurological Disorders and Animal Models

    DArcangelo, Gabriella / Merighi, Adalberto / Lossi, Laura

    2017  

    Abstract: The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of ... ...

    Abstract The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimers disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders
    Keywords Neurosciences. Biological psychiatry. Neuropsychiatry ; Science (General)
    Size 1 electronic resource (179 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020095033
    ISBN 9782889451111 ; 2889451119
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  6. Book: Cellular and molecular methods in neuroscience research

    Merighi, Adalberto

    2002  

    Author's details Adalberto Merighi ... ed
    Keywords Neurons / physiology ; Neurobiology / methods ; Nervenzelle ; Molekularbiologie ; Labormedizin ; Cytologie
    Subject Labordiagnostik ; Medizinische Labortechnik ; Laboratoriumsdiagnostik ; Laboratoriumsmedizin ; Zellbiologie ; Zellenlehre ; Zellforschung ; Zellkunde ; Zelluologie ; Zytologie ; Zelle ; Ganglienzelle ; Neurozyt ; Neuron ; Molekulare Biologie
    Language English
    Size XIII, 303 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT013628181
    ISBN 0-387-95386-8 ; 978-0-387-95386-1
    Database Catalogue ZB MED Medicine, Health

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  7. Article ; Online: Co-cultures of cerebellar slices from mice with different

    Merighi, Adalberto / Lossi, Laura

    F1000Research

    2023  Volume 11, Page(s) 1183

    Abstract: Background: ...

    Abstract Background:
    MeSH term(s) Animals ; Mice ; Cell Adhesion Molecules, Neuronal/genetics ; Cell Adhesion Molecules, Neuronal/metabolism ; Cerebellum ; Coculture Techniques ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism ; Reelin Protein/genetics
    Chemical Substances Cell Adhesion Molecules, Neuronal ; Extracellular Matrix Proteins ; Serine Endopeptidases (EC 3.4.21.-) ; Reln protein, mouse (EC 3.4.21.-) ; Reelin Protein
    Language English
    Publishing date 2023-10-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2699932-8
    ISSN 2046-1402 ; 2046-1402
    ISSN (online) 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.126787.2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: An Overview of the Epigenetic Modifications in the Brain under Normal and Pathological Conditions.

    Lossi, Laura / Castagna, Claudia / Merighi, Adalberto

    International journal of molecular sciences

    2024  Volume 25, Issue 7

    Abstract: Epigenetic changes are changes in gene expression that do not involve alterations to the DNA sequence. These changes lead to establishing a so-called epigenetic code that dictates which and when genes are activated, thus orchestrating gene regulation and ...

    Abstract Epigenetic changes are changes in gene expression that do not involve alterations to the DNA sequence. These changes lead to establishing a so-called epigenetic code that dictates which and when genes are activated, thus orchestrating gene regulation and playing a central role in development, health, and disease. The brain, being mostly formed by cells that do not undergo a renewal process throughout life, is highly prone to the risk of alterations leading to neuronal death and neurodegenerative disorders, mainly at a late age. Here, we review the main epigenetic modifications that have been described in the brain, with particular attention on those related to the onset of developmental anomalies or neurodegenerative conditions and/or occurring in old age. DNA methylation and several types of histone modifications (acetylation, methylation, phosphorylation, ubiquitination, sumoylation, lactylation, and crotonylation) are major players in these processes. They are directly or indirectly involved in the onset of neurodegeneration in Alzheimer's or Parkinson's disease. Therefore, this review briefly describes the roles of these epigenetic changes in the mechanisms of brain development, maturation, and aging and some of the most important factors dynamically regulating or contributing to these changes, such as oxidative stress, inflammation, and mitochondrial dysfunction.
    MeSH term(s) Brain ; Epigenesis, Genetic ; DNA Methylation ; Protein Processing, Post-Translational ; Acetylation
    Language English
    Publishing date 2024-03-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25073881
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Costorage of High Molecular Weight Neurotransmitters in Large Dense Core Vesicles of Mammalian Neurons.

    Merighi, Adalberto

    Frontiers in cellular neuroscience

    2018  Volume 12, Page(s) 272

    Abstract: It is today widely accepted that several types of high molecular weight (MW) neurotransmitters produced by neurons are synthesized at the cell body, selectively stored within large dense core vesicles (LDCVs) and anterogradely transported to terminals ... ...

    Abstract It is today widely accepted that several types of high molecular weight (MW) neurotransmitters produced by neurons are synthesized at the cell body, selectively stored within large dense core vesicles (LDCVs) and anterogradely transported to terminals where they elicit their biological role(s). Among these molecules there are neuropeptides and neurotrophic factors, the main focus of this perspective article. I here first provide a brief resume of the state of art on neuronal secretion, with primary emphasis on the molecular composition and mechanism(s) of filling and release of LDCVs. Then, I discuss the perspectives and future directions of research in the field as regarding the synthesis and storage of multiple high MW transmitters in LDCVs and the possibility that a selective sorting of LDCVs occurs along different neuronal processes and/or their branches. I also consider the ongoing discussion that diverse types of neurons may contain LDCVs with different sets of integral proteins or dial in a different fashion with LDCVs containing the same cargo. In addition, I provide original data on the size of LDCVs in rat dorsal root ganglion neurons and their central terminals in the spinal cord after immunogold labeling for calcitonin gene-related peptide (CGRP), neuropeptide K, substance P, neurokinin A or somatostatin. These data corroborate the idea that, similarly to endocrine cells, LDCVs undergo a process of maturation which involves a homotypic fusion followed by a reduction in size and condensation of cargo. They also give support to the conjecture that release at terminals occurs by cavicapture, a process of partial fusion of the vesicle with the axolemma, accompanied by depletion of cargo and diminution of size.
    Language English
    Publishing date 2018-08-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2018.00272
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The histology, physiology, neurochemistry and circuitry of the substantia gelatinosa Rolandi (lamina II) in mammalian spinal cord.

    Merighi, Adalberto

    Progress in neurobiology

    2018  Volume 169, Page(s) 91–134

    Abstract: The substantia gelatinosa Rolandi (SGR) was first described about two centuries ago. In the following decades an enormous amount of information has permitted us to understand - at least in part - its role in the initial processing of pain and itch. Here, ...

    Abstract The substantia gelatinosa Rolandi (SGR) was first described about two centuries ago. In the following decades an enormous amount of information has permitted us to understand - at least in part - its role in the initial processing of pain and itch. Here, I will first provide a comprehensive picture of the histology, physiology, and neurochemistry of the normal SGR. Then, I will analytically discuss the SGR circuits that have been directly demonstrated or deductively envisaged in the course of the intensive research on this area of the spinal cord, with particular emphasis on the pathways connecting the primary afferent fibers and the intrinsic neurons. The perspective existence of neurochemically-defined sets of primary afferent neurons giving rise to these circuits will be also discussed, with the proposition that a cross-talk between different subsets of peptidergic fibers may be the structural and functional substrate of additional gating mechanisms in SGR. Finally, I highlight the role played by slow acting high molecular weight modulators in these gating mechanisms.
    MeSH term(s) Animals ; History, 19th Century ; Humans ; Mammals ; Nerve Net/cytology ; Nerve Net/metabolism ; Nerve Net/physiology ; Neurochemistry/history ; Spinal Cord/anatomy & histology ; Substantia Gelatinosa/cytology ; Substantia Gelatinosa/physiology
    Language English
    Publishing date 2018-07-04
    Publishing country England
    Document type Historical Article ; Journal Article ; Review
    ZDB-ID 185535-9
    ISSN 1873-5118 ; 0301-0082
    ISSN (online) 1873-5118
    ISSN 0301-0082
    DOI 10.1016/j.pneurobio.2018.06.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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