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Bale M.R.,University of Manchester | Bale M.R.,Institute Neurociencias Of Alicante Umh Csic | Campagner D.,University of Manchester | Erskine A.,University of Manchester | And 2 more authors.
Journal of Neuroscience | Year: 2015

Communication in the nervous system occurs by spikes: the timing precision with which spikes are fired is a fundamental limit on neural information processing. In sensory systems, spike-timing precision is constrained by first-order neurons. We found that spike-timing precision of trigeminal primary afferents in rats and mice is limited both by stimulus speed and by electrophysiological sampling rate. High-speed video of behaving mice revealed whisker velocities of at least 17,000°/s, so we delivered an ultrafast “ping” (>50,000°/s) to single whiskers and sampled primary afferent activity at 500 kHz. Median spike jitter was 17.4 μs; 29% of neurons had spike jitter < 10 μs. These results indicate that the input stage of the trigeminal pathway has extraordinary spike-timing precision and very high potential information capacity. This timing precision ranks among the highest in biology. © 2015 the authors. Source


Maravall M.,Institute Neurociencias Of Alicante Umh Csic | Diamond M.E.,International School for Advanced Studies
Current Opinion in Neurobiology | Year: 2014

Comparison of the functional organization of sensory modalities can reveal the specialized mechanisms unique to each modality as well as processing algorithms that are common across modalities. Here we examine the rodent whisker system. The whisker's mechanical properties shape the forces transmitted to specialized receptors. The sensory and motor systems are intimately interconnected, giving rise to two forms of sensation: generative and receptive. The sensory pathway is a test bed for fundamental concepts in computation and coding: hierarchical feature detection, sparseness, adaptive representations, and population coding. The central processing of signals can be considered a sequence of filters. At the level of cortex, neurons represent object features by a coordinated population code which encompasses cells with heterogeneous properties. © 2014 Elsevier Ltd. Source


Bueno C.,Institute Neurociencias Of Alicante Umh Csic | Ramirez C.,Institute Neurociencias Of Alicante Umh Csic | Rodriguez-Lozano F.J.,University of Murcia | Tabares-Seisdedos R.,University of Valencia | And 4 more authors.
Cell Transplantation | Year: 2013

Previous studies suggest that neural crest (NC)-derived stem cells may reside in NC derivatives including the human periodontal ligament (hPDL). The isolation and manipulation of autologous NC-derived cells could be an accessible source of adult neural stem cells for their use in cell replacement and gene transfer to the diseased central nervous system. In this study, we examined the expression of NC markers and neural differentiation potential of hPDL-derived cells both in vitro and in vivo. In vitro we found that hPDL-derived cells expressed stem cell markers (Oct3/4, Nestin, Sox2, and Musashi-1) and a subset of NC cell markers (Slug, p75NTR, Twist, and Sox9). hPDL-derived cells differentiated into neural-like cells based on cellular morphology and neural marker expression (TUJ1, MAP2, MAP1b, GAD65/67, GABA, NeuN, ChAT, GAT1, synaptophysin, GFAP, NG2, and O4). In vivo, hPDL-derived cells survive, migrate, and give rise to DCX+, NF-M+, GABA+, GFAP+, and NG2+ cells after grafting the adult mouse brain. Some of the grafted hPDL-derived cells were located in stem cell niches such as the ventricular epithelium and the subventricular zone of the anterolateral ventricle wall as well as in the subgranular zone of the hippocampal dentate gyrus. Thus, the hPDL contains stem cells that originate from the NC and can differentiate into neural cells. The engraftment and differentiation properties of hPDL-derived cells in the adult brain indicate that they are a potential stem cell source to be used in neuroregenerative and/or neurotrophic medicine. © 2013 Cognizant Comm. Corp. Source


Valor L.M.,Institute Neurociencias Of Alicante Umh Csic | Jancic D.,Institute Neurociencias Of Alicante Umh Csic | Lujan R.,University of Castilla - La Mancha | Barco A.,Institute Neurociencias Of Alicante Umh Csic
Cell Death and Differentiation | Year: 2010

We compare here the neurodegenerative processes observed in the hippocampus of bitransgenic mice with chronically altered levels of cAMP-response element-binding protein (CREB) function. The combination of genome-wide transcriptional profiling of degenerating hippocampal tissue with microscopy analyses reveals that the sustained inhibition of CREB function in A-CREB mice is associated with dark neuron degeneration, whereas its strong chronic activation in VP16-CREB mice primarily causes excitotoxic cell death and inflammation. Furthermore, the meta-analysis with gene expression profiles available in public databases identifies relevant common markers to other neurodegenerative processes and highlights the importance of the immune response in neurodegeneration. Overall, these analyses define the ultrastructural and transcriptional signatures associated with these two forms of hippocampal neurodegeneration, confirm the importance of fine-tuned regulation of CREB-dependent gene expression for CA1 neuron survival and function, and provide novel insight into the function of CREB in the etiology of neurodegenerative processes. © 2010 Macmillan Publishers Limited All rights reserved. Source


Gomez-Sanchez J.A.,Institute Neurociencias Of Alicante Umh Csic | Gomez-Sanchez J.A.,Hospital General Universitario Of Alicante | Gomis-Coloma C.,Institute Neurociencias Of Alicante Umh Csic | Gomis-Coloma C.,Hospital General Universitario Of Alicante | And 5 more authors.
Brain | Year: 2013

The number of Schwann cells is fitted to axonal length in peripheral nerves. This relationship is lost when tumorigenic stimuli induce uncontrolled Schwann cell proliferation, generating tumours such us neurofibromas and schwannomas. Schwann cells also re-enter the cell cycle following nerve injury during the process of Wallerian degeneration. In both cases proliferation is finally arrested. We show that in neurofibroma, the induction of Jmjd3 (jumonji domain containing 3, histone lysine demethylase) removes trimethyl groups on lysine-27 of histone-H3 and epigenetically activates the Ink4a/Arf-locus, forcing Schwann cells towards replicative senescence. Remarkably, blocking this mechanism allows unrestricted proliferation, inducing malignant transformation of neurofibromas. Interestingly, our data suggest that in injured nerves, Schwann cells epigenetically activate the same locus to switch off proliferation and enter the senescence programme. Indeed, when this pathway is genetically blocked, Schwann cells fail to drop out of the cell cycle and continue to proliferate. We postulate that the Ink4a/Arf-locus is expressed as part of a physiological response that prevents uncontrolled proliferation of the de-differentiated Schwann cell generated during nerve regeneration, a response that is also activated to avoid overproliferation after tumorigenic stimuli in the peripheral nervous system. © 2013 The Author (2013). Source

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