125 research outputs found
sj-vid-1-phl-10.1177_0268355518805686 - Supplemental material for A novel endovenous scaffold for the treatment of chronic venous obstruction in a porcine model: Histological and ultrastructural assessment
No full textSupplemental material, sj-vid-1-phl-10.1177_0268355518805686 for A novel endovenous scaffold for the treatment of chronic venous obstruction in a porcine model: Histological and ultrastructural assessment by Paolo Zamboni, Alessia Giaquinta, Erika Rimondi, Massimo Pedriali, Eugenio Scanziani, Pietro Riccaboni, Massimiliano Veroux, Paola Secchiero and Pierfrancesco Veroux in Phlebology</p
sj-vid-2-phl-10.1177_0268355518805686 - Supplemental material for A novel endovenous scaffold for the treatment of chronic venous obstruction in a porcine model: Histological and ultrastructural assessment
No full textSupplemental material, sj-vid-2-phl-10.1177_0268355518805686 for A novel endovenous scaffold for the treatment of chronic venous obstruction in a porcine model: Histological and ultrastructural assessment by Paolo Zamboni, Alessia Giaquinta, Erika Rimondi, Massimo Pedriali, Eugenio Scanziani, Pietro Riccaboni, Massimiliano Veroux, Paola Secchiero and Pierfrancesco Veroux in Phlebology</p
Input normalization by global feedforward inhibition expands cortical dynamic range
No full textThe cortex is sensitive to weak stimuli, but responds to stronger inputs without saturating. The mechanisms that enable this wide range of operation are not fully understood. We found that the amplitude of excitatory synaptic currents necessary to fire rodent pyramidal cells, the threshold excitatory current, increased with stimulus strength. Consequently, the relative contribution of individual afferents in firing a neuron was inversely proportional to the total number of active afferents. Feedforward inhibition, acting homogeneously across pyramidal cells, ensured that threshold excitatory currents increased with stimulus strength. In contrast, heterogeneities in the distribution of excitatory currents in the neuronal population determined the specific set of pyramidal cells recruited. Together, these mechanisms expand the range of afferent input strengths that neuronal populations can represent.Fil: Pouille, Frédéric. University Of California. Department Of Neurobiology; Estados UnidosFil: Marin Burgin, Antonia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. University Of California. Department Of Neurobiology; Estados UnidosFil: Adesnik, Hillel. University Of California. Department Of Neurobiology; Estados UnidosFil: Atallah, Bassam V.. University Of California. Department Of Neurobiology; Estados UnidosFil: Scanziani, Massimo. University Of California. Department Of Neurobiology; Estados Unido
Dog as model for down-expression of E-cadherin and beta-catenin in tubular epithelial cells in renal fibrosis.
No full textMechanism of renal fibrosis leading to end stage kidney remains still a challenge of interest in humans. The pathogenesis of chronic kidney disease is characterized by progressive loss of kidney function and fibrosis. The mechanism of epithelial-mesenchymal transition (EMT) has been predominantly studied in in vitro studies, and we previously demonstrated the EMT of tubular epithelial cells in dogs. In this study, we examined and quantified the modifications of cadherin-catenin complex by immunohistochemistry of E-cadherin and beta-catenin and the mesenchymal marker vimentin in 25 dogs with three different spontaneous inflammatory renal diseases. Results showed a significant down-expression of levels of E-cadherin and beta-catenin directly correlated with the tubular-interstitial damage (TID). In TID grades 2 and 3, E-cadherin expression was significantly reduced (p < 0.001). beta-catenin expression was overall similar to E-cadherin. The mesenchymal-associated protein, vimentin, was de novo identified in tubules within areas of inflammation. In this work, we identified the loss of cadherin or catenin expression as a progressive mechanism in tubulo-interstitial fibrosis, which allows dissociation of structural integrity of renal epithelia and loss of epithelial polarity. The dog might result more significant as model for new therapies
A novel endovenous scaffold for the treatment of chronic venous obstruction in a porcine model: Histological and ultrastructural assessment
No full textObjective To investigate the biological effects of a novel endovenous scaffold in a porcine model. Methods Petalo is a compliant venous scaffold implanted into the internal jugular veins of 12 healthy pigs. The pigs were sacrificed at one, two, three, and six months, respectively. Microscopic investigations were performed at two blinded laboratories. Results Neo-intima formation progressively covering up the stent metallic bars was observed. The inflammatory response of the venous wall showed a peak after three months by the implant, followed by marked reduction after six months. The device induced a significant (p < 0.01) increase of the thickness respect to the control regions, but was comparable in sections obtained after three and six months. Conclusions The implant of Petalo compliant venous scaffold in the venous wall of this porcine model is characterized by neointima formation and by an inflammatory reaction which tends to decrease after six months. Our data point against the induction of smooth muscle cells proliferation and migration as confirmed by electronic transmission microscopy analyses
Développement et assemblage des circuits corticaux / Developmental assembly of cortical circuits
No full textSéminaire FSER organisé par Gordon Fishell (NYU Neuroscience Institute) du 9 au 14 mars 2015 Participants Alain Chédotal, Rosa Cossart, Sophie Deneve, Gordon Fishell, Sonia Garel, Anirvan Ghosh, Martyn Goulding, Kenneth Harris, Adam Kepecs, Attila Losonczy, Oscar Marin, Thomas Mrsic-Flogel, Franck Polleux, Nathalie Rochefort, Botond Roska, Bernardo Rudy, Scanziani Massimo -- Résumé Les recherches des dix dernières années ont vu l’émergence d’un nombre considérable de données relatives à l’ori..
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Cortical Dynamics in Visual Processing
No full textRecurrent circuits are a hallmark of mammalian sensory cortex. How they impact dynamics of sensory representation is not understood. Because recurrent circuits provide a majority of the synaptic excitation to cortical neurons in response to sensory stimulation, the intrinsic dynamics of these cortical recurrent circuits are expected to be a critical determinant of the timing of the sensory response in cortex. Previous methods could not isolate dynamics of these intra-cortical recurrent circuits from those of thalamic afferents during sensory processing. I now accomplish this by developing an approach to optogenetically silence thalamus in a model system: the mouse visual pathway. Silencing thalamus revealed the time course over which visually evoked activity in visual cortex was maintained by the intra-cortical recurrent circuits themselves, in isolation from thalamic input. I found that, at all time points during the cortical sensory-evoked response, optogenetically silencing thalamus led to a fast decay of sensory-evoked activity in cortical recurrent circuits. This activity decay time course was fit by a 10 ms network time constant, similar to a neuron’s integration time window. This decay time course was invariant across all tested visual stimulation conditions and behavioral states but depended on cortical inhibition. In awake mice, the dynamics of this time course predicted the time-locking of cortical activity to thalamic input at frequencies <15 Hz and the attenuation of the cortical response to higher frequencies. Under anesthesia, however, dynamics of depression at thalamocortical synapses disrupted the fidelity of sensory transmission. Thus, I determine sensory-evoked dynamics intrinsic to the intra-cortical recurrent circuits in isolation from thalamus and show how these dynamics transform afferent input in time
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Understanding cellular and behavioral consequences of Scn2a haploinsufficiency in cerebellar circuits
No full textEver since Hodgkin and Huxley described the sodium dependence in action potential nearly 70 years ago, neuroscientists have discovered an entire family of voltage-gated sodium channels (NaVs) in neuronal cells. Uncovering the differential distributions of these NaV isoforms between and within each type of neuron helped us understand the distinct roles they play in cellular functions. So crucial to normal neuronal physiology, genetic variants that result in protein structure changes can cause pronounced alteration in brain function and lead to disease. NaV1.2, encoded by SCN2A, is one NaV isoform whose genetic variants have been linked to neurodevelopmental disorders such as autism spectrum disorder (ASD). Studies have uncovered the importance of NaV1.2 in neuronal intrinsic properties and synaptic physiology in the forebrain. However, how these channels maintain normal cellular functions in the cerebellum, in which some of the strongest expression of NaV1.2 are detected, is unclear. The cerebellum is heavily implicated in ASD due to its functions in motor learning, fine movement control, and more recently discovered, cognition. Therefore, understanding how SCN2A dysfunctions alter cerebellar circuit has become critical to study disease manifestation in channelopathies. In my thesis work, I found that Scn2a haploinsufficiency in mice decreased cerebellar granule cell excitability, impaired high-frequency action potential propagation along their axons, and ultimately compromised the downstream synaptic plasticity that is critical to cerebellar learning. I also used cerebellum-dependent vestibulo-ocular reflex (VOR) to uncover that mice with Scn2a heterozygosity exhibited saturated VOR gain and deficit in VOR adaptation, which are correlated with abnormal Purkinje cell firing pattern during behavior. In addition, children with LoF SCN2A variants showed a similarly elevated baseline VOR gain. Lastly, I revealed that the VOR adaptation deficit in mice can be rescued by upregulating Scn2a in the entire mouse brain using a novel CRISPR activation technique. I hope this work will contribute to our understanding of sodium channel function in the cerebellum and ASD
GABA Spillover Activates Postsynaptic GABAB Receptors to Control Rhythmic Hippocampal Activity
No full textAbstractIn the hippocampus, interneurons provide synaptic inhibition via the transmitter GABA, which can activate GABAA and GABAB receptors (GABAARs and GABABRs). Generally, however, GABA released by a single interneuron activates only GABAARs on its targets, despite the abundance of GABABRs. Here, I show that during hippocampal rhythmic activity, simultaneous release of GABA from several interneurons activates postsynaptic GABABRs and that block of GABABRs increases oscillation frequency. Furthermore, if GABA uptake is inhibited, even GABA released by a single interneuron is enough to activate GABABRs. This occurs also on cells not directly contacted by that interneuron, indicating that GABA has to overcome uptake and exit the synaptic cleft to reach GABABRs. Thus, activation of extrasynaptic GABABRs by pooling of GABA is an important mechanism regulating hippocampal network activity
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