Alessandro Vercelli |
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Università degli Studi di Torino
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NICO - Neuroscience Institute Cavalieri Ottolenghi
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Research experience
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Jan 2009–
Dec 2012Research: Azienda Ospedaliero Universitaria Maggiore della Carità
Azienda Ospedaliero Universitaria Maggiore della CaritàNovara · Italy -
Jan 1991–
Dec 2012Research: Università degli Studi di Torino
Università degli Studi di Torino · Dipartimento di Psicologia, Dipartimento di Scienze Cliniche e Biologiche, Dipartimento di NeuroscienzeTorino · Italy -
Jan 2011
Research: Accademia di Agricoltura di Torino
Accademia di Agricoltura di TorinoTorino · Italy -
Jan 2011
Research: Azienda Ospedaliero Universitaria San Luigi Gonzaga
Azienda Ospedaliero Universitaria San Luigi GonzagaOrbassano · Italy -
Jan 2011
Research: Instituto de Biologia Experimental e Tecnológica IBET
Instituto de Biologia Experimental e Tecnológica IBETPortugal -
Jan 2010
Research: Karolinska Institutet
Karolinska Institutet · Institutionen för neurovetenskapSolna · Sweden -
Jan 2009
Research: Università degli Studi del Piemonte Orientale "Amedeo Avogadro"
Università degli Studi del Piemonte Orientale "Amedeo Avogadro"Alessandria · Italy -
Jan 2005
Research: Azienda Ospedaliero-Universitaria San Giovanni Battista di Torino
Azienda Ospedaliero-Universitaria San Giovanni Battista di TorinoTorino · Italy -
Jan 1990
Research: Ospedale Ordine Mauriziano di Torino, Umberto I
Ospedale Ordine Mauriziano di Torino, Umberto ITorino · Italy
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Teaching: Anatomy for Medical students
Education
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Oct 1990–
Sep 1992Université de Lausanne
PhDSwitzerland · Lausanne -
Jan 1987–
Dec 1990Università degli Studi di Torino
PhDItaly · Torino -
Oct 1980–
Jul 1986Università degli Studi di Torino
MDItaly · Torino
Other
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LanguagesItalian (Mother language), English and French
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Scientific MembershipsSFN, FENS, SINS, GISN
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Journal RefereesNeurobiology of Disease, PlosOne, European Journal of Neuroscience
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Other Interestspast SINS secretary
Secretary General GISN
Questions and Answers (1) View all
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Answer added in Neuroanatomy13 What is the best way to remove the vitreous body from the mouse retina?By Jens Hannibal · National Health ServiceAlessandro Vercelli · Università degli Studi di TorinoI used to fix the retina AFTER removal of the vitreous body. I cut the anterior segment, then made three radial cuts and then took out the vireous bod... [more]I used to fix the retina AFTER removal of the vitreous body. I cut the anterior segment, then made three radial cuts and then took out the vireous body; some vitreous remains attache do the retina, so I removed it mechanically with watchmaker's forceps... if you have to do electrophysiology, or immunohistochemistry, some vitreous can give problems, so I uses collagenase to dissolve it. Then I flattened the retina with the ganglion cell layer up on a slide, and then put some drops of fixative on it, and let the retina to fix for some hours at 4°C in a closed capsule, with some fixative around to prevent drying of the retina.Following
Publications (81) View all
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Article: The Diameter of Cortical Axons Depends Both on the Area of Origin and Target.
Giorgio M Innocenti, Alessandro Vercelli, Roberto Caminiti[show abstract] [hide abstract]
ABSTRACT: In primates, different cortical areas send axons of different diameters into comparable tracts, notably the corpus callosum (Tomasi S, Caminiti R, Innocenti GM. 2012. Areal differences in diameter and length of corticofugal projections. Cereb Cortex. 22:1463-1472). We now explored if an area also sends axons of different diameters to different targets. We find that the parietal area PEc sends thicker axons to area 4 and 6, and thinner ones to the cingulate region (area 24). Areas 4 and 9, each sends axons of different diameters to the nucleus caudatus, to different levels of the internal capsule, and to the thalamus. The internal capsule receives the thickest axon, followed by thalamus and nucleus caudatus. The 2 areas (4 and 9) differ in the diameter and length of axons to corresponding targets. We calculated how diameter determines conduction velocity of the axons and together with pathway length determines transmission delays between different brain sites. We propose that projections from and within the cerebral cortex consist of a complex system of lines of communication with different geometrical and time computing properties.Cerebral Cortex 03/2013; · 6.54 Impact Factor -
Article: Mesenchymal stem cell transplantation reduces glial cyst and improves functional outcome following spinal cord compression.
[show abstract] [hide abstract]
ABSTRACT: OBJECTIVE: Mesenchymal stem cells (MSCs) are multipotent stem cells that play a supportive role in regenerative therapies, especially in the CNS where spontaneous regeneration is limited. MSCs can exert a paracrine activity and modulate the inflammatory response after a CNS injury, Spinal cord injury (SCI) leads to permanent neurological deficits below the injury site, due to neuronal and axonal damage. Among the experimental treatments following SCI, cell transplantation emerged as a promising approach. METHODS: We used a compression injury model in the mouse spinal cord and we acutely transplanted MSCs into the lesion cavity; injured mice without the graft served as controls. After 26 days we investigated the survival of MSCs and evaluated their effect on the formation of the glial cyst and on injury-related inflammation. RESULTS: Grafted MSCs remained permanently undifferentiated. In MSC-treated mice the lesion volume was reduced by 31.6%, compared to control mice, despite astroglial and microglial activation was not altered by graft. Moreover sensory and motor tests demonstrated that MSC cell therapy results in improvement on a battery of behavioural tests, in comparison to control mice: in detail, MSC-treated mice vs control ones respectively registered the score 0.00 vs 0.50 in the posture test, 0.00 vs 1.50 in the hindlimb flexion test, 3.00 vs 2.25 in the sensory test, and finally 7.50 mistakes vs 15.83, respectively, in the foot-fault test. CONCLUSION: Our results underscore the therapeutic potential of MSCs, making them promising candidates for CNS pathologies.World Neurosurgery 09/2012; · 0.68 Impact Factor -
SourceAvailable from: Franco Cauda
Article: How many clusters in the insular cortex?
Franco Cauda, Alessandro VercelliCerebral Cortex 08/2012; · 6.54 Impact Factor -
Article: Role of JNK isoforms in the development of neuropathic pain following sciatic nerve transection in the mouse.
Giusi Manassero, Ivan E Repetto, Stefano Cobianchi, Valeria Valsecchi, Christophe Bonny, Ferdinando Rossi, Alessandro Vercelli[show abstract] [hide abstract]
ABSTRACT: Current tools for analgesia are often only partially successful, thus investigations of new targets for pain therapy stimulate great interest. Consequent to peripheral nerve injury, c-Jun N-terminal kinase (JNK) activity in cells of the dorsal root ganglia (DRGs) and spinal cord is involved in triggering neuropathic pain. However, the relative contribution of distinct JNK isoforms is unclear. Using knockout mice for single isoforms, and blockade of JNK activity by a peptide inhibitor, we have used behavioral tests to analyze the contribution of JNK in the development of neuropathic pain after unilateral sciatic nerve transection. In addition, immunohistochemical labelling for the growth associated protein (GAP)-43 and Calcitonin Gene Related Peptide (CGRP) in DRGs was used to relate injury related compensatory growth to altered sensory function. Peripheral nerve injury produced pain-related behavior on the ipsilateral hindpaw, accompanied by an increase in the percentage of GAP43-immunoreactive (IR) neurons and a decrease in the percentage of CGRP-IR neurons in the lumbar DRGs. The JNK inhibitor, D-JNKI-1, successfully modulated the effects of the sciatic nerve transection. The onset of neuropathic pain was not prevented by the deletion of a single JNK isoform, leading us to conclude that all JNK isoforms collectively contribute to maintain neuropathy. Autotomy behavior, typically induced by sciatic nerve axotomy, was absent in both the JNK1 and JNK3 knockout mice. JNK signaling plays an important role in regulating pain threshold: the inhibition of all of the JNK isoforms prevents the onset of neuropathic pain, while the deletion of a single splice JNK isoform mitigates established sensory abnormalities. JNK inactivation also has an effect on axonal sprouting following peripheral nerve injury.Molecular Pain 05/2012; 8(1):39. · 3.53 Impact Factor -
SourceAvailable from: Franco Cauda
Article: Meta-analytic clustering of the insular cortex: characterizing the meta-analytic connectivity of the insula when involved in active tasks.
Franco Cauda, Tommaso Costa, Diana M E Torta, Katiuscia Sacco, Federico D'Agata, Sergio Duca, Giuliano Geminiani, Peter T Fox, Alessandro Vercelli[show abstract] [hide abstract]
ABSTRACT: The human insula has been parcellated on the basis of resting state functional connectivity and diffusion tensor imaging. Little is known about the organization of the insula when involved in active tasks. We explored this issue using a novel meta-analytic clustering approach. We queried the BrainMap database asking for papers involving normal subjects that recorded activations in the insular cortex, retrieving 1305 papers, involving 22,872 subjects and a total of 2957 foci. Data were analyzed with several different methodologies, some of which expressly designed for this work. We used meta-analytic connectivity modeling and meta-analytic clustering of data obtained from the BrainMap database. We performed cluster analysis to subdivide the insula in areas with homogeneous connectivity, and density analysis of the activated foci using Voronoi tessellation. Our results confirm and extend previous findings obtained investigating the resting state connectivity of the anterior-posterior and left-right insulae. They indicate, for the first time, that some blocks of the anterior insula play the role of hubs between the anterior and the posterior insulae, as confirmed by their activation in several different paradigms. This finding supports the view that the network to which the anterior insula belongs is related to saliency detection. The insulae of both sides can be parcellated in two clusters, the anterior and the posterior: the anterior is characterized by an attentional pattern of connectivity with frontal, cingulate, parietal, cerebellar and anterior insular highly connected areas, whereas the posterior is characterized by a more local connectivity pattern with connections to sensorimotor, temporal and posterior cingulate areas. This antero-posterior subdivision, better characterized on the right side, results sharper with the connectivity based clusterization than with the behavioral based clusterization. The circuits belonging to the anterior insula are very homogeneous and their blocks in multidimensional scaling of MACM-based profiles are in central position, whereas those belonging to the posterior insula, especially on the left, are located at the periphery and sparse, thus suggesting that the posterior circuits bear a more heterogeneous connectivity. The anterior cluster is mostly activated by cognition, whereas the posterior is mostly activated by interoception, perception and emotion.NeuroImage 04/2012; 62(1):343-55. · 5.89 Impact Factor