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Prof. Adalberto Merighi
Department of Veterinary Sciences, University of Turin - Turin - Italy

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Article
Published: 03 July 2021 in Cellular and Molecular Neurobiology
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Pyramidal neurons (PNs) are the most abundant cells of the neocortex and display a vast dendritic tree, divided into basal and apical compartments. Morphological and functional anomalies of PN dendrites are at the basis of virtually all neurological and mental disorders, including intellectual disability. Here, we provide evidence that the cognitive deficits observed in different types of intellectual disability might be sustained by different parts of the PN dendritic tree, or by a dysregulation of their interaction.

ACS Style

Alberto Granato; Adalberto Merighi. Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability. Cellular and Molecular Neurobiology 2021, 1 -7.

AMA Style

Alberto Granato, Adalberto Merighi. Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability. Cellular and Molecular Neurobiology. 2021; ():1-7.

Chicago/Turabian Style

Alberto Granato; Adalberto Merighi. 2021. "Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability." Cellular and Molecular Neurobiology , no. : 1-7.

Preprint content
Published: 10 May 2021
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Pyramidal neurons (PNs) are the most abundant cells of the neocortex and display a vast dendritic tree, divided into basal and apical compartments. Morphological and functional anomalies of PN dendrites are at the basis of virtually all neurological and mental disorders, including intellectual disability. Here we provide evidence that the cognitive deficits observed in different types of intellectual disability might be sustained by different parts of the PN dendritic tree, or by a dysregulation of their interaction.

ACS Style

Alberto Granato; Adalberto Merighi. Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability. 2021, 1 .

AMA Style

Alberto Granato, Adalberto Merighi. Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability. . 2021; ():1.

Chicago/Turabian Style

Alberto Granato; Adalberto Merighi. 2021. "Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability." , no. : 1.

Short communication
Published: 03 March 2021 in Biochemistry and Biophysics Reports
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Ex vivo spinal cord slice cultures (SCSC) allow study of spinal cord circuitry, maintaining stimuli responses comparable to live animals. Previously, we have shown that mesenchymal stem/stromal cell (MSC) transplantation in vivo reduced inflammation and increased nerve regeneration but MSC survival was short-lived, highlighting that beneficial action may derive from the secretome. Previous in vitro studies of MSC conditioned medium (CM) have also shown increased neuronal growth. In this study, murine SCSC were cultured in canine MSC CM (harvested from the adipose tissue of excised inguinal fat) and cell phenotypes analysed via immunohistochemistry and confocal microscopy. SCSC in MSC CM displayed enhanced viability after propidium iodide staining. GFAP immunoreactivity was significantly increased in SCSC in MSC CM compared to controls, but with no change in proteoglycan (NG2) immunoreactivity. In contrast, culture in MSC CM significantly decreased the prevalence of βIII-tubulin immunoreactive neurites, whilst Ca2+ transients per cell were significantly increased. These ex vivo results contradict previous in vitro and in vivo reports of how MSC and their secretome may affect the microenvironment of the spinal cord after injury and highlight the importance of a careful comparison of the different experimental conditions used to assess the potential of cell therapies for the treatment of spinal cord injury.

ACS Style

Chelsea R. Wood; Esri H. Juárez; Francesco Ferrini; Peter Myint; John Innes; Laura Lossi; Adalberto Merighi; William E.B. Johnson. Mesenchymal stem cell conditioned medium increases glial reactivity and decreases neuronal survival in spinal cord slice cultures. Biochemistry and Biophysics Reports 2021, 26, 100976 .

AMA Style

Chelsea R. Wood, Esri H. Juárez, Francesco Ferrini, Peter Myint, John Innes, Laura Lossi, Adalberto Merighi, William E.B. Johnson. Mesenchymal stem cell conditioned medium increases glial reactivity and decreases neuronal survival in spinal cord slice cultures. Biochemistry and Biophysics Reports. 2021; 26 ():100976.

Chicago/Turabian Style

Chelsea R. Wood; Esri H. Juárez; Francesco Ferrini; Peter Myint; John Innes; Laura Lossi; Adalberto Merighi; William E.B. Johnson. 2021. "Mesenchymal stem cell conditioned medium increases glial reactivity and decreases neuronal survival in spinal cord slice cultures." Biochemistry and Biophysics Reports 26, no. : 100976.

Journal article
Published: 25 June 2020 in Molecules
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The interest in the biological properties of grapevine polyphenols (PPs) in neuroprotection is continuously growing in the hope of finding translational applications. However, there are several concerns about the specificity of action of these molecules that appear to act non-specifically on the permeability of cellular membranes. Naturally occurring neuronal death (NOND) during cerebellar maturation is a well characterized postnatal event that is very useful to investigate the death and rescue of neurons. We here aimed to establish a baseline comparative study of the potential to counteract NOND of certain grapevine PPs of interest for the oenology. To do so, we tested ex vivo the neuroprotective activity of peonidin- and malvidin-3-O-glucosides, resveratrol, polydatin, quercetin-3-O-glucoside, (+)-taxifolin, and (+)-catechin. The addition of these molecules (50 μM) to organotypic cultures of mouse cerebellum explanted at postnatal day 7, when NOND reaches a physiological peak, resulted in statistically significant (two-tailed Mann–Whitney test—p < 0.001) reductions of the density of dead cells (propidium iodide+ cells/mm2) except for malvidin-3-O-glucoside. The stilbenes were less effective in reducing cell death (to 51–60%) in comparison to flavanols, (+)-taxifolin and quercetin 3-O-glucoside (to 69–72%). Thus, molecules with a -OH group in ortho position (taxifolin, quercetin 3-O-glucoside, (+)-catechin, and peonidin 3-O-glucoside) have a higher capability to limit death of cerebellar neurons. As NOND is apoptotic, we speculate that PPs act by inhibiting executioner caspase 3.

ACS Style

Laura Lossi; Adalberto Merighi; Vittorino Novello; Alessandra Ferrandino. Protective Effects of Some Grapevine Polyphenols against Naturally Occurring Neuronal Death. Molecules 2020, 25, 2925 .

AMA Style

Laura Lossi, Adalberto Merighi, Vittorino Novello, Alessandra Ferrandino. Protective Effects of Some Grapevine Polyphenols against Naturally Occurring Neuronal Death. Molecules. 2020; 25 (12):2925.

Chicago/Turabian Style

Laura Lossi; Adalberto Merighi; Vittorino Novello; Alessandra Ferrandino. 2020. "Protective Effects of Some Grapevine Polyphenols against Naturally Occurring Neuronal Death." Molecules 25, no. 12: 2925.

Journal article
Published: 18 April 2020
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ACS Style

Chiara Salio; Patrizia Aimar; Pascale Malapert; Aziz Moqrich; Adalberto Merighi. Neurochemical and Ultrastructural Characterization of Unmyelinated Non-peptidergic C-Nociceptors and C-Low Threshold Mechanoreceptors Projecting to Lamina II of the Mouse Spinal Cord. 2020, 1 .

AMA Style

Chiara Salio, Patrizia Aimar, Pascale Malapert, Aziz Moqrich, Adalberto Merighi. Neurochemical and Ultrastructural Characterization of Unmyelinated Non-peptidergic C-Nociceptors and C-Low Threshold Mechanoreceptors Projecting to Lamina II of the Mouse Spinal Cord. . 2020; ():1.

Chicago/Turabian Style

Chiara Salio; Patrizia Aimar; Pascale Malapert; Aziz Moqrich; Adalberto Merighi. 2020. "Neurochemical and Ultrastructural Characterization of Unmyelinated Non-peptidergic C-Nociceptors and C-Low Threshold Mechanoreceptors Projecting to Lamina II of the Mouse Spinal Cord." , no. : 1.

Review
Published: 01 December 2019 in Journal of Clinical Medicine
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The first description of the Reeler mutation in mouse dates to more than fifty years ago, and later, its causative gene (reln) was discovered in mouse, and its human orthologue (RELN) was demonstrated to be causative of lissencephaly 2 (LIS2) and about 20% of the cases of autosomal-dominant lateral temporal epilepsy (ADLTE). In both human and mice, the gene encodes for a glycoprotein referred to as reelin (Reln) that plays a primary function in neuronal migration during development and synaptic stabilization in adulthood. Besides LIS2 and ADLTE, RELN and/or other genes coding for the proteins of the Reln intracellular cascade have been associated substantially to other conditions such as spinocerebellar ataxia type 7 and 37, VLDLR-associated cerebellar hypoplasia, PAFAH1B1-associated lissencephaly, autism, and schizophrenia. According to their modalities of inheritances and with significant differences among each other, these neuropsychiatric disorders can be modeled in the homozygous (reln−/−) or heterozygous (reln+/−) Reeler mouse. The worth of these mice as translational models is discussed, with focus on their construct and face validity. Description of face validity, i.e., the resemblance of phenotypes between the two species, centers onto the histological, neurochemical, and functional observations in the cerebral cortex, hippocampus, and cerebellum of Reeler mice and their human counterparts.

ACS Style

Laura Lossi; Claudia Castagna; Alberto Granato; Adalberto Merighi. The Reeler Mouse: A Translational Model of Human Neurological Conditions, or Simply a Good Tool for Better Understanding Neurodevelopment? Journal of Clinical Medicine 2019, 8, 2088 .

AMA Style

Laura Lossi, Claudia Castagna, Alberto Granato, Adalberto Merighi. The Reeler Mouse: A Translational Model of Human Neurological Conditions, or Simply a Good Tool for Better Understanding Neurodevelopment? Journal of Clinical Medicine. 2019; 8 (12):2088.

Chicago/Turabian Style

Laura Lossi; Claudia Castagna; Alberto Granato; Adalberto Merighi. 2019. "The Reeler Mouse: A Translational Model of Human Neurological Conditions, or Simply a Good Tool for Better Understanding Neurodevelopment?" Journal of Clinical Medicine 8, no. 12: 2088.

Original research
Published: 16 May 2019 in Cellular and Molecular Neurobiology
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Reeler heterozygous mice (reln+/-) are seemingly normal but haplodeficient in reln, a gene implicated in autism. Structural/neurochemical alterations in the reln+/- brain are subtle and difficult to demonstrate. Therefore, the usefulness of these mice in translational research is still debated. As evidence implicated several synapse-related genes in autism and the cerebellar vermis is structurally altered in the condition, we have investigated the expression of synaptophysin 1 (SYP1) and contactin 6 (CNTN6) within the vermis of reln+/- mice. Semi-thin plastic sections of the vermis from adult mice of both sexes and different genotypes (reln+/- and reln+/+) were processed with an indirect immunofluorescence protocol. Immunofluorescence was quantified on binary images and statistically analyzed. Reln+/- males displayed a statistically significant reduction of 11.89% in the expression of SYP1 compared to sex-matched wild-type animals, whereas no differences were observed between reln+/+ and reln+/- females. In reln+/- male mice, reductions were particularly evident in the molecular layer: 10.23% less SYP1 than reln+/+ males and 5.84% < reln+/+ females. In reln+/- females, decrease was 9.84% versus reln+/+ males and 5.43% versus reln+/+ females. Both reln+/- males and females showed a stronger decrease in CNTN6 expression throughout all the three cortical layers of the vermis: 17-23% in the granular layer, 24-26% in the Purkinje cell layer, and 9-14% in the molecular layer. Altogether, decrease of vermian SYP1 and CNTN6 in reln+/- mice displayed patterns compatible with the structural modifications of the autistic cerebellum. Therefore, these mice may be a good model in translational studies.

ACS Style

Claudia Castagna; Adalberto Merighi; Laura Lossi. Decreased Expression of Synaptophysin 1 (SYP1 Major Synaptic Vesicle Protein p38) and Contactin 6 (CNTN6/NB3) in the Cerebellar Vermis of reln Haplodeficient Mice. Cellular and Molecular Neurobiology 2019, 39, 833 -856.

AMA Style

Claudia Castagna, Adalberto Merighi, Laura Lossi. Decreased Expression of Synaptophysin 1 (SYP1 Major Synaptic Vesicle Protein p38) and Contactin 6 (CNTN6/NB3) in the Cerebellar Vermis of reln Haplodeficient Mice. Cellular and Molecular Neurobiology. 2019; 39 (6):833-856.

Chicago/Turabian Style

Claudia Castagna; Adalberto Merighi; Laura Lossi. 2019. "Decreased Expression of Synaptophysin 1 (SYP1 Major Synaptic Vesicle Protein p38) and Contactin 6 (CNTN6/NB3) in the Cerebellar Vermis of reln Haplodeficient Mice." Cellular and Molecular Neurobiology 39, no. 6: 833-856.

Review
Published: 12 December 2018 in International Journal of Molecular Sciences
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Caspase-3, onto which there is a convergence of the intrinsic and extrinsic apoptotic pathways, is the main executioner of apoptosis. We here review the current literature on the intervention of the protease in the execution of naturally occurring neuronal death (NOND) during cerebellar development. We will consider data on the most common altricial species (rat, mouse and rabbit), as well as humans. Among the different types of neurons and glia in cerebellum, there is ample evidence for an intervention of caspase-3 in the regulation of NOND of the post-mitotic cerebellar granule cells (CGCs) and Purkinje neurons, as a consequence of failure to establish proper synaptic contacts with target (secondary cell death). It seems possible that the GABAergic interneurons also undergo a similar type of secondary cell death, but the intervention of caspase-3 in this case still remains to be clarified in full. Remarkably, CGCs also undergo primary cell death at the precursor/pre-migratory stage of differentiation, in this instance without the intervention of caspase-3. Glial cells, as well, undergo a process of regulated cell death, but it seems possible that expression of caspase-3, at least in the Bergmann glia, is related to differentiation rather than death.

ACS Style

Laura Lossi; Claudia Castagna; Adalberto Merighi. Caspase-3 Mediated Cell Death in the Normal Development of the Mammalian Cerebellum. International Journal of Molecular Sciences 2018, 19, 3999 .

AMA Style

Laura Lossi, Claudia Castagna, Adalberto Merighi. Caspase-3 Mediated Cell Death in the Normal Development of the Mammalian Cerebellum. International Journal of Molecular Sciences. 2018; 19 (12):3999.

Chicago/Turabian Style

Laura Lossi; Claudia Castagna; Adalberto Merighi. 2018. "Caspase-3 Mediated Cell Death in the Normal Development of the Mammalian Cerebellum." International Journal of Molecular Sciences 19, no. 12: 3999.

Perspective article
Published: 21 August 2018 in Frontiers in Cellular Neuroscience
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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.

ACS Style

Adalberto Merighi. Costorage of High Molecular Weight Neurotransmitters in Large Dense Core Vesicles of Mammalian Neurons. Frontiers in Cellular Neuroscience 2018, 12, 272 .

AMA Style

Adalberto Merighi. Costorage of High Molecular Weight Neurotransmitters in Large Dense Core Vesicles of Mammalian Neurons. Frontiers in Cellular Neuroscience. 2018; 12 ():272.

Chicago/Turabian Style

Adalberto Merighi. 2018. "Costorage of High Molecular Weight Neurotransmitters in Large Dense Core Vesicles of Mammalian Neurons." Frontiers in Cellular Neuroscience 12, no. : 272.

Review article
Published: 19 July 2018 in Frontiers in Veterinary Science
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The principles of the 3Rs—Replacement, Reduction, and Refinement—are at the basis of most advanced national and supranational (EU) regulations on animal experimentation and welfare. In the perspective to reduce and refine the use of these animals in translational research, we here discuss the use of rodent acute and organotypically cultured central nervous system slices. We describe novel applications of these ex vivo platforms in medium-throughput screening of neuroactive molecules of potential pharmacological interest, with particular attention to more recent developments that permit to fully exploit the potential of direct genetic engineering of organotypic cultures using transfection techniques. We then describe the perspectives for expanding the use ex vivo platforms in neuroscience studies under the 3Rs philosophy using the following approaches: (1) Use of co-cultures of two brain regions physiologically connected to each other (source-target) to analyze axon regeneration and reconstruction of circuitries; (2) Microinjection or co-cultures of primary cells and/or cell lines releasing one or more neuroactive molecules to screen their physiological and/or pharmacological effects onto neuronal survival and slice circuitry. Microinjected or co-cultured cells are ideally made fluorescent after transfection with a plasmid construct encoding green or red fluorescent protein under the control of a general promoter such as hCMV; (3) Use of “sniffer” cells sensing the release of biologically active molecules from organotypic cultures by means of fluorescent probes. These cells can be prepared with activatable green fluorescent protein, a unique chromophore that remains in a “dark” state because its maturation is inhibited, and can be made fluorescent (de-quenched) if specific cellular enzymes, such as proteases or kinases, are activated.

ACS Style

Laura Lossi; Adalberto Merighi. The Use of ex Vivo Rodent Platforms in Neuroscience Translational Research With Attention to the 3Rs Philosophy. Frontiers in Veterinary Science 2018, 5, 1 .

AMA Style

Laura Lossi, Adalberto Merighi. The Use of ex Vivo Rodent Platforms in Neuroscience Translational Research With Attention to the 3Rs Philosophy. Frontiers in Veterinary Science. 2018; 5 ():1.

Chicago/Turabian Style

Laura Lossi; Adalberto Merighi. 2018. "The Use of ex Vivo Rodent Platforms in Neuroscience Translational Research With Attention to the 3Rs Philosophy." Frontiers in Veterinary Science 5, no. : 1.

Review article
Published: 04 July 2018 in Progress in Neurobiology
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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 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 fibers 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.

ACS Style

Adalberto Merighi. The histology, physiology, neurochemistry and circuitry of the substantia gelatinosa Rolandi (lamina II) in mammalian spinal cord. Progress in Neurobiology 2018, 169, 91 -134.

AMA Style

Adalberto Merighi. The histology, physiology, neurochemistry and circuitry of the substantia gelatinosa Rolandi (lamina II) in mammalian spinal cord. Progress in Neurobiology. 2018; 169 ():91-134.

Chicago/Turabian Style

Adalberto Merighi. 2018. "The histology, physiology, neurochemistry and circuitry of the substantia gelatinosa Rolandi (lamina II) in mammalian spinal cord." Progress in Neurobiology 169, no. : 91-134.

Protocol
Published: 06 October 2017 in Animal Models of Drug Addiction
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Brain-derived neurotrophic factor (BDNF) exerts its trophic and neuromodulatory effects by acting on the high-affinity specific receptor trkB. To obtain precise information on the subcellular localization of BDNF and trkB receptors in neurons and their synapses we here present two immunohistochemical techniques used for ultrastructural investigations: a post-embedding immunogold staining protocol for detecting BDNF and a pre-embedding Fluoronanogold™ immunostaining method to detect trkB receptors, by using secondary fluorescein-tagged antibodies conjugated with ultrasmall gold particles. Moreover, we describe here how to combine the two procedures in the same tissue samples for BDNF/trkB multiple labelling studies.

ACS Style

Chiara Salio; Adalberto Merighi. Ultrastructural Localization of BDNF and trkB Receptors. Animal Models of Drug Addiction 2017, 133 -148.

AMA Style

Chiara Salio, Adalberto Merighi. Ultrastructural Localization of BDNF and trkB Receptors. Animal Models of Drug Addiction. 2017; ():133-148.

Chicago/Turabian Style

Chiara Salio; Adalberto Merighi. 2017. "Ultrastructural Localization of BDNF and trkB Receptors." Animal Models of Drug Addiction , no. : 133-148.

Review
Published: 23 May 2017 in BMC Neurology
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Vascular cognitive impairment (VCI) is a heterogeneous entity with multiple aetiologies, all linked to underlying vascular disease. Among these, VCI related to subcortical small vessel disease (SSVD) is emerging as a major homogeneous subtype. Its progressive course raises the need for biomarker identification and/or development for adequate therapeutic interventions to be tested. In order to shed light in the current status on biochemical markers for VCI-SSVD, experts in field reviewed the recent evidence and literature data. The group conducted a comprehensive search on Medline, PubMed and Embase databases for studies published until 15.01.2017. The proposal on current status of biochemical markers in VCI-SSVD was reviewed by all co-authors and the draft was repeatedly circulated and discussed before it was finalized. This review identifies a large number of biochemical markers derived from CSF and blood. There is a considerable overlap of VCI-SSVD clinical symptoms with those of Alzheimer’s disease (AD). Although most of the published studies are small and their findings remain to be replicated in larger cohorts, several biomarkers have shown promise in separating VCI-SSVD from AD. These promising biomarkers are closely linked to underlying SSVD pathophysiology, namely disruption of blood-CSF and blood–brain barriers (BCB-BBB) and breakdown of white matter myelinated fibres and extracellular matrix, as well as blood and brain inflammation. The leading biomarker candidates are: elevated CSF/blood albumin ratio, which reflects BCB/BBB disruption; altered CSF matrix metalloproteinases, reflecting extracellular matrix breakdown; CSF neurofilment as a marker of axonal damage, and possibly blood inflammatory cytokines and adhesion molecules. The suggested SSVD biomarker deviations contrasts the characteristic CSF profile in AD, i.e. depletion of amyloid beta peptide and increased phosphorylated and total tau. Combining SSVD and AD biomarkers may provide a powerful tool to identify with greater precision appropriate patients for clinical trials of more homogeneous dementia populations. Thereby, biomarkers might promote therapeutic progress not only in VCI-SSVD, but also in AD.

ACS Style

A. Wallin; E. Kapaki; M. Boban; S. Engelborghs; D. M. Hermann; B. Huisa; M. Jonsson; M. G. Kramberger; L. Lossi; B. Malojcic; S. Mehrabian; A. Merighi; E. B. Mukaetova-Ladinska; G. P. Paraskevas; B. O. Popescu; R. Ravid; L. Traykov; G. Tsivgoulis; G. Weinstein; A. Korczyn; M. Bjerke; G. Rosenberg. Biochemical markers in vascular cognitive impairment associated with subcortical small vessel disease - A consensus report. BMC Neurology 2017, 17, 1 -12.

AMA Style

A. Wallin, E. Kapaki, M. Boban, S. Engelborghs, D. M. Hermann, B. Huisa, M. Jonsson, M. G. Kramberger, L. Lossi, B. Malojcic, S. Mehrabian, A. Merighi, E. B. Mukaetova-Ladinska, G. P. Paraskevas, B. O. Popescu, R. Ravid, L. Traykov, G. Tsivgoulis, G. Weinstein, A. Korczyn, M. Bjerke, G. Rosenberg. Biochemical markers in vascular cognitive impairment associated with subcortical small vessel disease - A consensus report. BMC Neurology. 2017; 17 (1):1-12.

Chicago/Turabian Style

A. Wallin; E. Kapaki; M. Boban; S. Engelborghs; D. M. Hermann; B. Huisa; M. Jonsson; M. G. Kramberger; L. Lossi; B. Malojcic; S. Mehrabian; A. Merighi; E. B. Mukaetova-Ladinska; G. P. Paraskevas; B. O. Popescu; R. Ravid; L. Traykov; G. Tsivgoulis; G. Weinstein; A. Korczyn; M. Bjerke; G. Rosenberg. 2017. "Biochemical markers in vascular cognitive impairment associated with subcortical small vessel disease - A consensus report." BMC Neurology 17, no. 1: 1-12.

Neuroscience
Published: 05 January 2017 in Frontiers in Cellular Neuroscience
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ACS Style

Gabriella D'Arcangelo; Laura Lossi; Adalberto Merighi. Editorial: Reelin-Related Neurological Disorders and Animal Models. Frontiers in Cellular Neuroscience 2017, 10, 1 .

AMA Style

Gabriella D'Arcangelo, Laura Lossi, Adalberto Merighi. Editorial: Reelin-Related Neurological Disorders and Animal Models. Frontiers in Cellular Neuroscience. 2017; 10 ():1.

Chicago/Turabian Style

Gabriella D'Arcangelo; Laura Lossi; Adalberto Merighi. 2017. "Editorial: Reelin-Related Neurological Disorders and Animal Models." Frontiers in Cellular Neuroscience 10, no. : 1.

Book chapter
Published: 01 January 2017 in Reference Module in Neuroscience and Biobehavioral Psychology
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Neuropeptides are small proteins produced by neurons that act on G protein-coupled receptors and are responsible for slow-onset, long-lasting modulation of synaptic transmission. Neuropeptides often coexist with each other or with other neurotransmitters in single neurons. According to their chemical nature, coexisting messengers are localized to different cell compartments: neuropeptides are packaged in large granular vesicles (LGVs), whereas low-molecular weight neurotransmitters are stored in small synaptic vesicles. This compartmentalization allows selective release in response to stimuli. Individual LGVs may store several different neuropeptides, at times with monoamines or neurotrophic factors. LGVs release their neuropeptide cargo by cavicapture or full-fusion exocytosis.

ACS Style

Adalberto Merighi. Neuropeptides and Coexistence ☆. Reference Module in Neuroscience and Biobehavioral Psychology 2017, 1 .

AMA Style

Adalberto Merighi. Neuropeptides and Coexistence ☆. Reference Module in Neuroscience and Biobehavioral Psychology. 2017; ():1.

Chicago/Turabian Style

Adalberto Merighi. 2017. "Neuropeptides and Coexistence ☆." Reference Module in Neuroscience and Biobehavioral Psychology , no. : 1.

Research article
Published: 01 January 2017 in Molecular Pain
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Presynaptic GABAB receptors (GABABRs) are highly expressed in dorsal root ganglion neurons and spinal cord dorsal horn. GABABRs located in superficial dorsal horn play an important antinociceptive role, by acting at both pre- and postsynaptic sites. GABABRs expressed in deep dorsal horn could be involved in the processing of touch sensation and possibly in the generation of tactile allodynia in chronic pain. The objective of this study was to characterize the morphological and functional properties of GABABRs expressed on Aβ fibers projecting to lamina III/IV and to understand their role in modulating excitatory synaptic transmission. We performed high-resolution electron microscopic analysis, showing that GABAB2 subunit is expressed on 71.9% of terminals in rat lamina III-IV. These terminals were engaged in axodendritic synapses and, for the 46%, also expressed glutamate immunoreactivity. Monosynaptic excitatory postsynaptic currents, evoked by Aβ fiber stimulation and recorded from lamina III/IV neurons in spinal cord slices, were strongly depressed by application of baclofen (0.1–2.5 µM), acting as a presynaptic modulator. Application of the GABABR antagonist CGP 55845 caused, in a subpopulation of neurons, the potentiation of the first of two excitatory postsynaptic currents recorded with the paired-pulse protocol, showing that GABABRs are endogenously activated. A decrease in the paired-pulse ratio accompanied the effect of CGP 55845, implying the involvement of presynaptic GABABRs. CGP 55845 facilitated only the first excitatory postsynaptic current also during a train of four consecutive stimuli applied to Aβ fibers. These results suggest that GABABRs tonically inhibit glutamate release from Aβ fibers at a subset of synapses in deep dorsal horn. This modulation specifically affects only the early phase of synaptic excitation in lamina III-IV neurons.

ACS Style

Chiara Salio; Adalberto Merighi; Rita Bardoni. GABABreceptors-mediated tonic inhibition of glutamate release from Aβ fibers in rat laminae III/IV of the spinal cord dorsal horn. Molecular Pain 2017, 13, 1 .

AMA Style

Chiara Salio, Adalberto Merighi, Rita Bardoni. GABABreceptors-mediated tonic inhibition of glutamate release from Aβ fibers in rat laminae III/IV of the spinal cord dorsal horn. Molecular Pain. 2017; 13 ():1.

Chicago/Turabian Style

Chiara Salio; Adalberto Merighi; Rita Bardoni. 2017. "GABABreceptors-mediated tonic inhibition of glutamate release from Aβ fibers in rat laminae III/IV of the spinal cord dorsal horn." Molecular Pain 13, no. : 1.

Journal article
Published: 01 September 2016 in Annals of Anatomy - Anatomischer Anzeiger
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Programmed cell death (PCD) was demonstrated in neurons and glia in normal brain development, plasticity, and aging, but also in neurodegeneration. (Macro)autophagy, characterized by cytoplasmic vacuolization and activation of lysosomal hydrolases, and apoptosis, typically entailing cell shrinkage, chromatin and nuclear condensation, are the two more common forms of PCD. Their underlying intracellular pathways are partly shared and neurons can die following both modalities, according to the type of death-triggering stimulus. Reelin is an extracellular protein necessary for proper neuronal migration and brain lamination. In the mutant Reeler mouse, its absence causes neuronal mispositioning, with a notable degree of cerebellar hypoplasia that was tentatively related to an increase in PCD. We have carried out an ultrastructural analysis on the occurrence and type of postnatal PCD affecting the cerebellar neurons in normal and Reeler mice. In the forming cerebellar cortex, PCD took the form of apoptosis or autophagy and mainly affected the cerebellar granule cells (CGCs). Densities of apoptotic CGCs were comparable in both mouse strains at P0-P10, while, in mutants, they increased to become significantly higher at P15. In WT mice the density of autophagic neurons did not display statistically significant differences in the time interval examined in this study, whereas it was reduced in Reeler in the P0-P10 interval, but increased at P15. Besides CGCs, the Purkinje neurons also displayed autophagic features in both WT and Reeler mice. Therefore, cerebellar neurons undergo different types of PCD and a Reelin deficiency affects the type and degree of neuronal death during postnatal development of the cerebellum.

ACS Style

Claudia Castagna; Adalberto Merighi; Laura Lossi. Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice. Annals of Anatomy - Anatomischer Anzeiger 2016, 207, 76 -90.

AMA Style

Claudia Castagna, Adalberto Merighi, Laura Lossi. Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice. Annals of Anatomy - Anatomischer Anzeiger. 2016; 207 ():76-90.

Chicago/Turabian Style

Claudia Castagna; Adalberto Merighi; Laura Lossi. 2016. "Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice." Annals of Anatomy - Anatomischer Anzeiger 207, no. : 76-90.

Journal article
Published: 01 September 2016 in Annals of Anatomy - Anatomischer Anzeiger
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The Reeler heterozygous mice (reln+/−) are haplodeficient in the gene (reln) encoding for the reelin glycoprotein (RELN) and display reductions in brain/peripheral RELN similar to autistic or schizophrenic patients. Cytoarchitectonic alterations of the reln+/− brain may be subtle, and are difficult to demonstrate by current histological approaches. We analyzed the number and topological organization of the Purkinje neurons (PNs) in five vermal lobules - central (II-III), culmen (IV-V), tuber (VIIb), uvula (IX), and nodulus (X) - that process different types of afferent functional inputs in reln+/+ and reln+/− adult mice (P60) of both sexes (n = 24). Animals were crossed with L7GFP mice so that the GFP-tagged PNs could be directly identified in cryosections. Digital images from these sections were processed with different open source software for quantitative topological and statistical analyses. Diversity indices calculated were: maximum caliper, density, area of soma, dispersion along the XZ axis, and dispersion along the YZ axis. We demonstrate: i. reduction in density of PNs in reln+/− males (14.37%) and reln+/− females (17.73%) compared to reln+/+ males; ii. that reln+/− males have larger PNs than other genotypes, and females (irrespective of the reln genetic background) have smaller PNs than reln+/+ males; iii. PNs are more chaotically arranged along the YZ axis in reln+/− males than in reln+/+ males and, except in central lobulus, reln+/− females. Therefore, image processing and statistics reveal previously unforeseen gender and genotype-related structural differences in cerebellum that may be clues for the definition of novel biomarkers in human psychiatric disorders.

ACS Style

Chiara Magliaro; Carolina Cocito; Stefano Bagatella; Adalberto Merighi; Arti Ahluwalia; Laura Lossi. The number of Purkinje neurons and their topology in the cerebellar vermis of normal and reln haplodeficient mouse. Annals of Anatomy - Anatomischer Anzeiger 2016, 207, 68 -75.

AMA Style

Chiara Magliaro, Carolina Cocito, Stefano Bagatella, Adalberto Merighi, Arti Ahluwalia, Laura Lossi. The number of Purkinje neurons and their topology in the cerebellar vermis of normal and reln haplodeficient mouse. Annals of Anatomy - Anatomischer Anzeiger. 2016; 207 ():68-75.

Chicago/Turabian Style

Chiara Magliaro; Carolina Cocito; Stefano Bagatella; Adalberto Merighi; Arti Ahluwalia; Laura Lossi. 2016. "The number of Purkinje neurons and their topology in the cerebellar vermis of normal and reln haplodeficient mouse." Annals of Anatomy - Anatomischer Anzeiger 207, no. : 68-75.

Journal article
Published: 01 September 2016 in Annals of Anatomy - Anatomischer Anzeiger
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ACS Style

Adalberto Merighi; Paolo De Girolamo. Editorial. Annals of Anatomy - Anatomischer Anzeiger 2016, 207, 1 .

AMA Style

Adalberto Merighi, Paolo De Girolamo. Editorial. Annals of Anatomy - Anatomischer Anzeiger. 2016; 207 ():1.

Chicago/Turabian Style

Adalberto Merighi; Paolo De Girolamo. 2016. "Editorial." Annals of Anatomy - Anatomischer Anzeiger 207, no. : 1.

Journal article
Published: 29 June 2016 in European Journal of Neuroscience
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The nociceptive system of rodents is not fully developed and functional at birth. Specifically, C fibers transmitting peripheral nociceptive information establish synaptic connections in the spinal cord already during the embryonic period that only become fully functional after birth. Here, we studied the consequences of neonatal maternal deprivation (NMD, 3h/day, P2-P12) on the functional establishment of C fiber-mediated neurotransmission in spinal cord and of pain-related behavior. In vivo recording revealed that C fiber-mediated excitation of spinal cord neurons could be observed at P14 only in control but not in NMD rats. NMD was associated with a strong alteration in the expression of growth factors controlling C nociceptor maturation as well as K2P channels known to set nociceptive thresholds. In good agreement, C-type sensory neurons from NMD animals appeared to be hypoexcitable but functionally connected to spinal neurons, especially those expressing TRPV1 receptors. In vivo and in vitro recordings of lamina II spinal neurons at P14 revealed that the NMD-related lack of C fiber-evoked responses resulted from an inhibitory barrage in the spinal cord dorsal horn. Eventually, C-type sensory-spinal processing could be recovered after a delay of about ten days in NMD animals. However, animals remained hypersensitive to noxious stimulus up to P100 and this might be due to an excessive expression of Nav1.8 transcripts in DRG neurons. Together, our data provide evidence for a deleterious impact of perinatal stress exposure on the maturation of the sensory-spinal nociceptive system that may contribute to the nociceptive hypersensitivity in early adulthood. This article is protected by copyright. All rights reserved.

ACS Style

Pierre-Eric Juif; Chiara Salio; Vivien Zell; Meggane Melchior; Adrien Lacaud; Nathalie Petit-Demouliere; Francesco Ferrini; Pascal Darbon; Ulrike Hanesch; Fernand Anton; Adalberto Merighi; Vincent Lelievre; Pierrick Poisbeau. Peripheral and central alterations affecting spinal nociceptive processing and pain at adulthood in rats exposed to neonatal maternal deprivation. European Journal of Neuroscience 2016, 44, 1952 -62.

AMA Style

Pierre-Eric Juif, Chiara Salio, Vivien Zell, Meggane Melchior, Adrien Lacaud, Nathalie Petit-Demouliere, Francesco Ferrini, Pascal Darbon, Ulrike Hanesch, Fernand Anton, Adalberto Merighi, Vincent Lelievre, Pierrick Poisbeau. Peripheral and central alterations affecting spinal nociceptive processing and pain at adulthood in rats exposed to neonatal maternal deprivation. European Journal of Neuroscience. 2016; 44 (3):1952-62.

Chicago/Turabian Style

Pierre-Eric Juif; Chiara Salio; Vivien Zell; Meggane Melchior; Adrien Lacaud; Nathalie Petit-Demouliere; Francesco Ferrini; Pascal Darbon; Ulrike Hanesch; Fernand Anton; Adalberto Merighi; Vincent Lelievre; Pierrick Poisbeau. 2016. "Peripheral and central alterations affecting spinal nociceptive processing and pain at adulthood in rats exposed to neonatal maternal deprivation." European Journal of Neuroscience 44, no. 3: 1952-62.