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  • 1. Bartoletti, Alessandro
    et al.
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Berardi, Nicoletta
    Maffei, Lamberto
    Environmental enrichment prevents effects of dark-rearing in the rat visual cortex2004In: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, Vol. 7, no 3, p. 215-216Article in journal (Refereed)
    Abstract [en]

    Environmental enrichment potentiates neural plasticity, enhancing acquisition and consolidation of memory traces. In the sensory cortices, after cortical circuit maturation and sensory function acquisition are completed, neural plasticity declines and the critical period 'closes'. In the visual cortex, this process can be prevented by dark-rearing, and here we show that environmental enrichment can promote physiological maturation and consolidation of visual cortical connections in dark-reared rats, leading to critical period closure.

  • 2. Blau, Axel
    et al.
    Murr, Angelika
    Wolff, Sandra
    Sernagor, Evelyne
    Medini, Paolo
    Iurilli, Giuliano
    Ziegler, Christiane
    Benfenati, Fabio
    Flexible, all-polymer microelectrode arrays for the capture of cardiac and neuronal signals2011In: Biomaterials, ISSN 0142-9612, E-ISSN 1878-5905, Vol. 32, no 7, p. 1778-1786Article in journal (Refereed)
    Abstract [en]

    Microelectrode electrophysiology has become a widespread technique for the extracellular recording of bioelectrical signals. To date, electrodes are made of metals or inorganic semiconductors, or hybrids thereof. We demonstrate that these traditional conductors can be completely substituted by highly flexible electroconductive polymers. Pursuing a two-level replica-forming strategy, conductive areas for electrodes, leads and contact pads are defined as microchannels in poly(dimethylsiloxane) (PDMS) as a plastic carrier and track insulation material. These channels are coated by films of organic conductors such as polystyrenesulfonate-doped poly(3,4-ethylenedioxy-thiophene) (PEDOT:PSS) or filled with a graphite-PDMS (gPDMS) composite, either alone or in combination. The bendable, somewhat stretchable, non-cytotoxic and biostable all-polymer microelectrode arrays (polyMEAs) with a thickness below 500 μm and up to 60 electrodes reliably capture action potentials (APs) and local field potentials (LFPs) from acute preparations of heart muscle cells and retinal whole mounts, in vivo epicortical and epidural recordings as well as during long-term in vitro recordings from cortico-hippocampal co-cultures.

  • 3. Iurilli, Giuliano
    et al.
    Benfenati, Fabio
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Loss of Visually Driven Synaptic Responses in Layer 4 Regular-Spiking Neurons of Rat Visual Cortex in Absence of Competing Inputs2012In: Cerebral Cortex, ISSN 1047-3211, E-ISSN 1460-2199, Vol. 22, no 9, p. 2171-2181Article in journal (Refereed)
    Abstract [en]

    Monocular deprivation (MD) during development shifts the ocular preference of primary visual cortex (V1) neurons by depressing closed-eye responses and potentiating open-eye responses. As these 2 processes are temporally and mechanistically distinct, we tested whether loss of responsiveness occurs also in absence of competing inputs. We thus compared the effects of long-term MD in layer 4 regular-spiking pyramidal neurons (L4Ns) of binocular and monocular V1 (bV1 and mV1) with whole-cell recordings. In bV1, input depression was larger than potentiation, and the ocular dominance shift was larger for spike outputs. MD-but not retinal inactivation with tetrodotoxin-caused a comparable loss of synaptic and spike responsiveness in mV1, which is innervated only by the deprived eye. Conversely, brief MD depressed synaptic responses only in bV1. MD-driven depression in mV1 was accompanied by a proportional reduction of visual thalamic inputs, as assessed upon pharmacological silencing of intracortical transmission. Finally, sub- and suprathreshold responsiveness was similarly degraded in L4Ns of bV1 upon complete deprivation of patterned vision through a binocular deprivation period of comparable length. Thus, loss of synaptic inputs from the deprived eye occurs also in absence of competition in the main thalamorecipient lamina, albeit at a slower pace.

  • 4. Iurilli, Giuliano
    et al.
    Ghezzi, Diego
    Olcese, Umberto
    Lassi, Glenda
    Nazzaro, Cristiano
    Tonini, Raffaella
    Tucci, Valter
    Benfenati, Fabio
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Sound-Driven Synaptic Inhibition in Primary Visual Cortex2012In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 73, no 4, p. 814-28Article in journal (Refereed)
    Abstract [en]

    Multimodal objects and events activate many sensory cortical areas simultaneously. This is possibly reflected in reciprocal modulations of neuronal activity, even at the level of primary cortical areas. However, the synaptic character of these interareal interactions, and their impact on synaptic and behavioral sensory responses are unclear. Here, we found that activation of auditory cortex by a noise burst drove local GABAergic inhibition on supragranular pyramids of the mouse primary visual cortex, via cortico-cortical connections. This inhibition was generated by sound-driven excitation of a limited number of cells in infragranular visual cortical neurons. Consequently, visually driven synaptic and spike responses were reduced upon bimodal stimulation. Also, acoustic stimulation suppressed conditioned behavioral responses to a dim flash, an effect that was prevented by acute blockade of GABAergic transmission in visual cortex. Thus, auditory cortex activation by salient stimuli degrades potentially distracting sensory processing in visual cortex by recruiting local, translaminar, inhibitory circuits.

  • 5.
    Iurilli, Giuliano
    et al.
    Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
    Olcese, Umberto
    Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
    Medini, Paolo
    Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
    Preserved Excitatory-Inhibitory Balance of Cortical Synaptic Inputs following Deprived Eye Stimulation after a Saturating Period of Monocular Deprivation in Rats2013In: PloS one, ISSN 1932-6203, Vol. 8, no 12, p. e82044-Article in journal (Refereed)
    Abstract [en]

    Monocular deprivation (MD) during development leads to a dramatic loss of responsiveness through the deprived eye in primary visual cortical neurons, and to degraded spatial vision (amblyopia) in all species tested so far, including rodents. Such loss of responsiveness is accompanied since the beginning by a decreased excitatory drive from the thalamo-cortical inputs. However, in the thalamorecipient layer 4, inhibitory interneurons are initially unaffected by MD and their synapses onto pyramidal cells potentiate. It remains controversial whether ocular dominance plasticity similarly or differentially affects the excitatory and inhibitory synaptic conductances driven by visual stimulation of the deprived eye and impinging onto visual cortical pyramids, after a saturating period of MD. To address this issue, we isolated visually-driven excitatory and inhibitory conductances by in vivo whole-cell recordings from layer 4 regular-spiking neurons in the primary visual cortex (V1) of juvenile rats. We found that a saturating period of MD comparably reduced visually-driven excitatory and inhibitory conductances driven by visual stimulation of the deprived eye. Also, the excitatory and inhibitory conductances underlying the synaptic responses driven by the ipsilateral, left open eye were similarly potentiated compared to controls. Multiunit recordings in layer 4 followed by spike sorting indicated that the suprathreshold loss of responsiveness and the MD-driven ocular preference shifts were similar for narrow spiking, putative inhibitory neurons and broad spiking, putative excitatory neurons. Thus, by the time the plastic response has reached a plateau, inhibitory circuits adjust to preserve the normal balance between excitation and inhibition in the cortical network of the main thalamorecipient layer.

  • 6. Mazzaro, Nadia
    et al.
    Barini, Erica
    Spillantini, Maria Grazia
    Goedert, Michel
    Medini, Paolo
    Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, 16163 Genova, Italy.
    Gasparini, Laura
    Tau-Driven Neuronal and Neurotrophic Dysfunction in a Mouse Model of Early Tauopathy2016In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 36, no 7, p. 2086-2100Article in journal (Refereed)
    Abstract [en]

    Tauopathies are neurodegenerative diseases characterized by intraneuronal inclusions of hyperphosphorylated tau protein and abnormal expression of brain-derived neurotrophic factor (BDNF), a key modulator of neuronal survival and function. The severity of both these pathological hallmarks correlate with the degree of cognitive impairment in patients. However, how tau pathology specifically modifies BDNF signaling and affects neuronal function during early prodromal stages of tauopathy remains unclear. Here, we report that the mild tauopathy developing in retinal ganglion cells (RGCs) of the P301S tau transgenic (P301S) mouse induces functional retinal changes by disrupting BDNF signaling via the TrkB receptor. In adult P301S mice, the physiological visual response of RGCs to pattern light stimuli and retinal acuity decline significantly. As a consequence, the activity-dependent secretion of BDNF in the vitreous is impaired in P301S mice. Further, in P301S retinas, TrkB receptors are selectively upregulated, but uncoupled from downstream extracellular signal-regulated kinase (ERK) 1/2 signaling. We also show that the impairment of TrkB signaling is triggered by tau pathology and mediates the tau-induced dysfunction of visual response. Overall our results identify a neurotrophin-mediated mechanism by which tau induces neuronal dysfunction during prodromal stages of tauopathy and define tau-driven pathophysiological changes of potential value to support early diagnosis and informed therapeutic decisions.

  • 7.
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Cell-type-specific sub- and suprathreshold receptive fields of layer 4 and layer 2/3 pyramids in rat primary visual cortex.2011In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 190, p. 112-26Article in journal (Refereed)
    Abstract [en]

    Connectivity of cortical pyramidal neurons is layer-specific in the primary visual cortex (V1) and this is thought to be reflected in different receptive field (RF) properties of layer 4 and layer 2/3 pyramidal neurons (L4Ps and L2/3Ps, respectively). However, it remains unclear how the two cell populations convert incoming visually driven synaptic inputs into action potential (AP) outputs. Here I compared postsynaptic potentials (PSPs) and AP responses of L4Ps and L2/3Ps in the binocular portion of rat V1 by intrinsic optical imaging (IOI)-targeted whole-cell recordings followed by anatomical identification and dendritic reconstructions. L2/3Ps had about 2-fold longer dendritic branches and a higher number of branch points and endings in their apical portions. Functionally, L2/3Ps had more hyperpolarized resting potentials and lower rates of spontaneous APs (medians: 0.07 vs. 0.60 AP/s). PSP responses to optimally oriented moving bars were comparable in terms of amplitude (16.0±0.9 vs. 17.3±1.1 mV for L2/3Ps and L4Ps, respectively), reliability and size of the RF. The modulated component of subthreshold responses of L4Ps to optimal sinusoidal drifting gratings was larger and their PSP onset latency in response to bars flashed in the cell's RF center were shorter (60 vs. 86 ms). In contrast to the similarities of PSP responses to moving bars, AP responses of L2/3Ps were more sparse (medians: 0.7 vs. 2.9 APs/stimulus passage), less reliable, but sharper in terms of angular size. Based on the differences of subthreshold inputs, I conclude that L4Ps may receive mostly thalamic inputs, whereas L2/3Ps may receive both thalamic and cortical inputs from layer 4. The comparable subthreshold responses to moving bars are converted by L2/3Ps into sparser but sharper AP outputs possibly by cell-type-specific AP-generating mechanisms or differences in visually driven inhibitory inputs.

  • 8.
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Experience-dependent plasticity of visual cortical microcircuits2014In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 278, p. 367-384Article, review/survey (Refereed)
    Abstract [en]

    The recent decade testified a tremendous increase in our knowledge on how cell-type-specific microcircuits process sensory information in the neocortex and on how such circuitry reacts to manipulations of the sensory environment. Experience-dependent plasticity has now been investigated with techniques endowed with cell resolution during both postnatal development and in adult animals. This review recapitulates the main recent findings in the field using mainly the primary visual cortex as a model system to highlight the more important questions and physiological principles (such as the role of non-competitive mechanisms, the role of inhibition in excitatory cell plasticity, the functional importance of spine and axonal plasticity on a microscale level). I will also discuss on which scientific problems the debate and controversies are more pronounced. New technologies that allow to perturbate cell-type-specific subcircuits will certainly shine new light in the years to come at least on some of the still open questions. (C) 2014 The Author. Published by Elsevier Ltd. on behalf of IBRO.

  • 9.
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Layer- and Cell-Type-Specific Subthreshold and Suprathreshold Effects of Long-Term Monocular Deprivation in Rat Visual Cortex2011In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 31, no 47, p. 17134-17148Article in journal (Refereed)
    Abstract [en]

    Connectivity and dendritic properties are determinants of plasticity that are layer and cell-type specific in the neocortex. However, the impact of experience-dependent plasticity at the level of synaptic inputs and spike outputs remains unclear along vertical cortical microcircuits. Here I compared subthreshold and suprathreshold sensitivity to prolonged monocular deprivation (MD) in rat binocular visual cortex in layer 4 and layer 2/3 pyramids (4Ps and 2/3Ps) and in thick-tufted and nontufted layer 5 pyramids (5TPs and 5NPs), which innervate different extracortical targets. In normal rats, 5TPs and 2/3Ps are the most binocular in terms of synaptic inputs, and 5NPs are the least. Spike responses of all 5TPs were highly binocular, whereas those of 2/3Ps were dominated by either the contralateral or ipsilateral eye. MD dramatically shifted the ocular preference of 2/3Ps and 4Ps, mostly by depressing deprived-eye inputs. Plasticity was profoundly different in layer 5. The subthreshold ocular preference shift was sevenfold smaller in 5TPs because of smaller depression of deprived inputs combined with a generalized loss of responsiveness, and was undetectable in 5NPs. Despite their modest ocular dominance change, spike responses of 5TPs consistently lost their typically high binocularity during MD. The comparison of MD effects on 2/3Ps and 5TPs, the main affected output cells of vertical microcircuits, indicated that subthreshold plasticity is not uniquely determined by the initial degree of input binocularity. The data raise the question of whether 5TPs are driven solely by 2/3Ps during MD. The different suprathreshold plasticity of the two cell populations could underlie distinct functional deficits in amblyopia.

  • 10.
    Medini, Paolo
    et al.
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Pizzorusso, Tommaso
    Visual experience and plasticity of the visual cortex: a role for epigenetic mechanisms2008In: Frontiers in bioscience : a journal and virtual library, ISSN 1093-4715, Vol. 13, p. 3000-3007Article in journal (Refereed)
    Abstract [en]

    Plasticity of cortical circuits is maximal during critical periods of postnatal development. Ocular dominance plasticity is a classical model to understand the role of experience in development of the visual cortex. Recent studies are beginning to unravel the synaptic mechanisms underlying this form of plasticity and to elucidate the different plasticity of juvenile and adult animals at mechanistic and molecular level. These investigations indicate that this form of plasticity is regulated by factors located at extracellular and intracellular level. The molecular composition of the extracellular environment in which synaptic plasticity occurs changes during development becoming less permissive for plasticity. In addition, visual experience activates epigenetic mechanisms of regulation of gene transcription that becomes downregulated in adult animals.

  • 11. Olcese, Umberto
    et al.
    Iurilli, Giuliano
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Cellular and synaptic architecture of multisensory integration in the mouse neocortex2013In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 79, no 3, p. 579-593Article in journal (Refereed)
    Abstract [en]

    Multisensory integration (MI) is crucial for sensory processing, but it is unclear how MI is organized in cortical microcircuits. Whole-cell recordings in a mouse visuotactile area located between primary visual and somatosensory cortices revealed that spike responses were less bimodal than synaptic responses but displayed larger multisensory enhancement. MI was layer and cell type specific, with multisensory enhancement being rare in the major class of inhibitory interneurons and in the output infragranular layers. Optogenetic manipulation of parvalbumin-positive interneuron activity revealed that the scarce MI of interneurons enables MI in neighboring pyramids. Finally, single-cell resolution calcium imaging revealed a gradual merging of modalities: unisensory neurons had higher densities toward the borders of the primary cortices, but were located in unimodal clusters in the middle of the cortical area. These findings reveal the role of different neuronal subcircuits in the synaptic process of MI in the rodent parietal cortex.

  • 12. Pizzorusso, Tommaso
    et al.
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Berardi, Nicoletta
    Chierzi, Sabrina
    Fawcett, James W
    Maffei, Lamberto
    Reactivation of ocular dominance plasticity in the adult visual cortex2002In: Science, ISSN 0036-8075, E-ISSN 1095-9203, Vol. 298, no 5596, p. 1248-51Article in journal (Refereed)
    Abstract [en]

    In young animals, monocular deprivation leads to an ocular dominance shift, whereas in adults after the critical period there is no such shift. Chondroitin sulphate proteoglycans (CSPGs) are components of the extracellular matrix (ECM) inhibitory for axonal sprouting. We tested whether the developmental maturation of the ECM is inhibitory for experience-dependent plasticity in the visual cortex. The organization of CSPGs into perineuronal nets coincided with the end of the critical period and was delayed by dark rearing. After CSPG degradation with chondroitinase-ABC in adult rats, monocular deprivation caused an ocular dominance shift toward the nondeprived eye. The mature ECM is thus inhibitory for experience-dependent plasticity, and degradation of CSPGs reactivates cortical plasticity.

  • 13. Pizzorusso, Tommaso
    et al.
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Landi, Silvia
    Baldini, Sara
    Berardi, Nicoletta
    Maffei, Lamberto
    Structural and functional recovery from early monocular deprivation in adult rats2006In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 103, no 22, p. 8517-8522Article in journal (Refereed)
    Abstract [en]

    Visual deficits caused by abnormal visual experience during development are hard to recover in adult animals. Removal of chondroitin sulfate proteoglycans from the mature extracellular matrix with chondroitinase ABC promotes plasticity in the adult visual cortex. We tested whether chondroitinase ABC treatment of adult rats facilitates anatomical, functional, and behavioral recovery from the effects of a period of monocular deprivation initiated during the critical period for monocular deprivation. We found that chondroitinase ABC treatment coupled with reverse lid-suturing causes a complete recovery of ocular dominance, visual acuity, and dendritic spine density in adult rats. Thus, manipulations of the extracellular matrix can be used to promote functional recovery in the adult cortex.

  • 14. Sale, Alessandro
    et al.
    Maya Vetencourt, José Fernando
    Medini, Paolo
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Cenni, Maria Cristina
    Baroncelli, Laura
    De Pasquale, Roberto
    Maffei, Lamberto
    Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition2007In: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, Vol. 10, no 6, p. 679-681Article in journal (Refereed)
    Abstract [en]

    Loss of visual acuity caused by abnormal visual experience during development (amblyopia) is an untreatable pathology in adults. We report that environmental enrichment in adult amblyopic rats restored normal visual acuity and ocular dominance. These effects were due to reduced GABAergic inhibition in the visual cortex, accompanied by increased expression of BDNF and reduced density of extracellular-matrix perineuronal nets, and were prevented by enhancement of inhibition through benzodiazepine cortical infusion.

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