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The lizard cerebral cortex as a model to study neuronal regeneration
LOPEZ-GARCIA, CARLOS;MOLOWNY, ASUNCION;NACHER, JUAN;PONSODA, XAVIER;SANCHO-BIELSA, FRANCISCO;ALONSO-LLOSA, GREGORI;
Anais da Academia Brasileira de Ciências , 2002, DOI: 10.1590/S0001-37652002000100006
Abstract: the medial cerebral cortex of lizards, an area homologous to the hippocampal fascia dentata, shows delayed postnatal neurogenesis, i.e., cells in the medial cortex ependyma proliferate and give rise to immature neurons, which migrate to the cell layer. there, recruited neurons differentiate and give rise to zinc containing axons directed to the rest of cortical areas, thus resulting in a continuous growth of the medial cortex and its zinc-enriched axonal projection. this happens along the lizard life span, even in adult lizards, thus allowing one of their most important characteristics: neuronal regeneration. experiments in our laboratory have shown that chemical lesion of the medial cortex (affecting up to 95% of its neurons) results in a cascade of events: first, massive neuronal death and axonal-dendritic retraction and, secondly, triggered ependymal-neuroblast proliferation and subsequent neo-histogenesis and regeneration of an almost new medial cortex, indistinguishable from a normal undamaged one. this is the only case to our knowledge of the regeneration of an amniote central nervous centre by new neuron production and neo-histogenesis. thus the lizard cerebral cortex is a good model to study neuronal regeneration and the complex factors that regulate its neurogenetic, migratory and neo-synaptogenetic events.
The lizard cerebral cortex as a model to study neuronal regeneration  [cached]
LOPEZ-GARCIA CARLOS,MOLOWNY ASUNCION,NACHER JUAN,PONSODA XAVIER
Anais da Academia Brasileira de Ciências , 2002,
Abstract: The medial cerebral cortex of lizards, an area homologous to the hippocampal fascia dentata, shows delayed postnatal neurogenesis, i.e., cells in the medial cortex ependyma proliferate and give rise to immature neurons, which migrate to the cell layer. There, recruited neurons differentiate and give rise to zinc containing axons directed to the rest of cortical areas, thus resulting in a continuous growth of the medial cortex and its zinc-enriched axonal projection. This happens along the lizard life span, even in adult lizards, thus allowing one of their most important characteristics: neuronal regeneration. Experiments in our laboratory have shown that chemical lesion of the medial cortex (affecting up to 95% of its neurons) results in a cascade of events: first, massive neuronal death and axonal-dendritic retraction and, secondly, triggered ependymal-neuroblast proliferation and subsequent neo-histogenesis and regeneration of an almost new medial cortex, indistinguishable from a normal undamaged one. This is the only case to our knowledge of the regeneration of an amniote central nervous centre by new neuron production and neo-histogenesis. Thus the lizard cerebral cortex is a good model to study neuronal regeneration and the complex factors that regulate its neurogenetic, migratory and neo-synaptogenetic events.
Does cell lineage in the developing cerebral cortex contribute to its columnar organization?  [PDF]
Marcos R. Costa,Cecilia Hedin-Pereira
Frontiers in Neuroanatomy , 2010, DOI: 10.3389/fnana.2010.00026
Abstract: Since the pioneer work of Lorente de Nó, Ramón y Cajal, Brodmann, Mountcastle, Hubel and Wiesel and others, the cerebral cortex has been seen as a jigsaw of anatomic and functional modules involved in the processing of different sets of information. In fact, a columnar distribution of neurons displaying similar functional properties throughout the cerebral cortex has been observed by many researchers. Although it has been suggested that much of the anatomical substrate for such organization would be already specified at early developmental stages, before activity-dependent mechanisms could take place, it is still unclear whether gene expression in the ventricular zone (VZ) could play a role in the development of discrete functional units, such as minicolumns or columns. Cell lineage experiments using replication-incompetent retroviral vectors have shown that the progeny of a single neuroepithelial/radial glial cell in the dorsal telencephalon is organized into discrete radial clusters of sibling excitatory neurons, which have a higher propensity for developing chemical synapses with each other rather than with neighboring non-siblings. Here, we will discuss the possibility that the cell lineage of single neuroepithelial/radial glia cells could contribute for the columnar organization of the neocortex by generating radial columns of sibling, interconnected neurons. Borrowing some concepts from the studies on cell–cell recognition and transcription factor networks, we will also touch upon the potential molecular mechanisms involved in the establishment of sibling-neuron circuits.
Fast Growth May Impair Regeneration Capacity in the Branching Coral Acropora muricata  [PDF]
Vianney Denis, Mireille M. M. Guillaume, Madeleine Goutx, Stéphane de Palmas, Julien Debreuil, Andrew C. Baker, Roxane K. Boonstra, J. Henrich Bruggemann
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072618
Abstract: Regeneration of artificially induced lesions was monitored in nubbins of the branching coral Acropora muricata at two reef-flat sites representing contrasting environments at Réunion Island (21°07′S, 55°32′E). Growth of these injured nubbins was examined in parallel, and compared to controls. Biochemical compositions of the holobiont and the zooxanthellae density were determined at the onset of the experiment, and the photosynthetic efficiency (Fv/Fm) of zooxanthellae was monitored during the experiment. Acropora muricata rapidly regenerated small lesions, but regeneration rates significantly differed between sites. At the sheltered site characterized by high temperatures, temperature variations, and irradiance levels, regeneration took 192 days on average. At the exposed site, characterized by steadier temperatures and lower irradiation, nubbins demonstrated fast lesion repair (81 days), slower growth, lower zooxanthellae density, chlorophyll a concentration and lipid content than at the former site. A trade-off between growth and regeneration rates was evident here. High growth rates seem to impair regeneration capacity. We show that environmental conditions conducive to high zooxanthellae densities in corals are related to fast skeletal growth but also to reduced lesion regeneration rates. We hypothesize that a lowered regenerative capacity may be related to limited availability of energetic and cellular resources, consequences of coral holobionts operating at high levels of photosynthesis and associated growth.
Spatial Stereoresolution for Depth Corrugations May Be Set in Primary Visual Cortex  [PDF]
Fredrik Allenmark ,Jenny C. A. Read
PLOS Computational Biology , 2011, DOI: 10.1371/journal.pcbi.1002142
Abstract: Stereo “3D” depth perception requires the visual system to extract binocular disparities between the two eyes' images. Several current models of this process, based on the known physiology of primary visual cortex (V1), do this by computing a piecewise-frontoparallel local cross-correlation between the left and right eye's images. The size of the “window” within which detectors examine the local cross-correlation corresponds to the receptive field size of V1 neurons. This basic model has successfully captured many aspects of human depth perception. In particular, it accounts for the low human stereoresolution for sinusoidal depth corrugations, suggesting that the limit on stereoresolution may be set in primary visual cortex. An important feature of the model, reflecting a key property of V1 neurons, is that the initial disparity encoding is performed by detectors tuned to locally uniform patches of disparity. Such detectors respond better to square-wave depth corrugations, since these are locally flat, than to sinusoidal corrugations which are slanted almost everywhere. Consequently, for any given window size, current models predict better performance for square-wave disparity corrugations than for sine-wave corrugations at high amplitudes. We have recently shown that this prediction is not borne out: humans perform no better with square-wave than with sine-wave corrugations, even at high amplitudes. The failure of this prediction raised the question of whether stereoresolution may actually be set at later stages of cortical processing, perhaps involving neurons tuned to disparity slant or curvature. Here we extend the local cross-correlation model to include existing physiological and psychophysical evidence indicating that larger disparities are detected by neurons with larger receptive fields (a size/disparity correlation). We show that this simple modification succeeds in reconciling the model with human results, confirming that stereoresolution for disparity gratings may indeed be limited by the size of receptive fields in primary visual cortex.
Formoterol May Activate Rat Muscle Regeneration During Cancer Cachexia  [cached]
Elisabet Ametller,Sílvia Busquets,Gemma Fuster,Maria T. Figueras
Insciences Journal , 2011,
Abstract: PURPOSE: The development of cancer cachexia is the most common manifestation of advanced malignant disease. METHOD: The effects on muscle regeneration of 2-adrenoceptor agonist formoterol (0.3 mg/kg) were tested in cachectic tumour-bearing rats (Yoshida AH-130 ascites hepatoma). RESULTS: Administration of formoterol results in a significant increase in the mass and protein content of tibialis muscle in tumour-bearing-rats. This increase is associated with a decreased myogenin mRNA content together with an increased Pax-7 gene expression. Bupivacaine treatment by local injection results in an important reduction in tibialis weight together with significant increases in Pax-7, myogenin and MyoD gene expression. Formoterol treatment in bupivacaine-treated rats results in significant increases in Pax-7 together with significant decreases in myogenin mRNA content, suggesting that this 2-agonist is favouring muscle regeneration by stimulating the proliferation of satellite cells.Altogether, the data reinforce the potential role of formoterol in the treatment of muscle wasting diseases.
Influence of Inflammation on Poststroke Plasticity  [PDF]
Monika Liguz-Lecznar,Malgorzata Kossut
Neural Plasticity , 2013, DOI: 10.1155/2013/258582
Abstract: Age-related brain injuries including stroke are a leading cause of morbidity and mental disability worldwide. Most patients who survive stroke experience some degree of recovery. The restoration of lost functions can be explained by neuronal plasticity, understood as brain ability to reorganize and remodel itself in response to changed environmental requirements. However, stroke triggers a cascade of events which may prevent the normal development of the plastic changes. One of them may be inflammatory response initiated immediately after stroke, which has been found to contribute to neuronal injury. Some recent evidence though has suggested that inflammatory reaction can be also neuroprotective. This paper attempts to discuss the influence of poststroke inflammatory response on brain plasticity and stroke outcome. We also describe the recent anti-inflammatory strategies that have been effective for recovery in experimental stroke. 1. Introduction Ischemic stroke results from two main pathological processes: a loss of oxygen and an interruption of glucose supply to a particular brain region. The collapse of energy provision leads to the dysfunction of ionic pumps, loss of membrane potential, and uncontrolled release of neurotransmitters. The consequence of those processes is the increase of intracellular calcium concentrations that, among many deleterious effects, result in the generation of free radicals, leading to disintegration of cell membranes and subsequent neuronal death in the core of infarction [1]. Necrosis in the center of infarction can start a few minutes after stroke and is followed by peri-infarct depolarizations, excitotoxicity, edema, and oxidative stress [2]. The more delayed processes accompanying stroke are inflammation and apoptosis. They are initiated several hours after ischemic attack and can persist even for several weeks [3]. Although a great progress has been made in understanding the cellular and molecular mechanisms of ischemic tissue damage, the only approved therapy is still thrombolysis achieved by intravenous administration of recombinant tissue plasminogen activator (tPA). Unfortunately, short therapeutic window for this therapy strongly limits the fraction of patient that can benefit from the treatment. Moreover, stroke induces a complex cascade of inflammatory response which contributes to the postischemic damage. The complex nature of phenomena after ischemic event hampers a successful design of effective therapeutic strategies (Figure 1). Figure 1: Acute cerebral ischemia, neuroinflammation, and plasticity.
Selective and constructive mechanisms contribute to neural circuit formation in the barrel cortex of the developing rat  [PDF]
Eileen Uribe-Querol, Eduardo Martínez-Martínez, Luis Rodrigo Hernández, Patricia Padilla Cortés, Horacio Merchant-Larios, Gabriel Gutiérrez-Ospinac
Advances in Bioscience and Biotechnology (ABB) , 2013, DOI: 10.4236/abb.2013.47103
Abstract: The cellular strategy leading to formation of neuronal circuits in the rodent barrel cortex is still a matter of controversy. Both selective and constructive mechanisms have been proposed. The selective mechanism involves an overproduction of neuronal processes and synapses followed by activity dependent pruning. Conversely, a constructive mechanism would increase the number of axons, dendrites, and synapses during development to match functionality. In order to discern the contributions of these two mechanisms in establishing a neuronal circuit in the somatosensory cortex, morphometric analysis of dendritic and axonal arbor growth was performed. Also, the number of synapses was followed by electron microscopy during the first month of life. We observed that axonal and dendritic arbors retracted distal branches, and elongated proximal branches, resulting in increased arbor complexity. This neuronal remodeling was accompanied by the steady increase in the number of synapses within barrel hollows. Similarly, the content of molecular markers for dendrites, axons and synapses also increased during this period. Finally, cytochrome oxidase activity rose with age in barrels indicating that the arbors became more complex while synapse density and metabolic demands increased. Our results support the simultaneous use of both selective and constructive mechanisms in establishing the barrel cortex circuitry.

Stellate Cells from Rat Pancreas Are Stem Cells and Can Contribute to Liver Regeneration  [PDF]
Claus Kordes, Iris Sawitza, Silke G?tze, Dieter H?ussinger
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051878
Abstract: The identity of pancreatic stem/progenitor cells is still under discussion. They were suggested to derive from the pancreatic ductal epithelium and/or islets. Here we report that rat pancreatic stellate cells (PSC), which are thought to contribute to pancreatic fibrosis, have stem cell characteristics. PSC reside in islets and between acini and display a gene expression pattern similar to umbilical cord blood stem cells and mesenchymal stem cells. Cytokine treatment of isolated PSC induced the expression of typical hepatocyte markers. The PSC-derived hepatocyte-like cells expressed endodermal proteins such as bile salt export pump along with the mesodermal protein vimentin. The transplantation of culture-activated PSC from enhanced green fluorescent protein-expressing rats into wild type rats after partial hepatectomy in the presence of 2-acetylaminofluorene revealed that PSC were able to reconstitute large areas of the host liver through differentiation into hepatocytes and cholangiocytes. This developmental fate of transplanted PSC was confirmed by fluorescence in situ hybridization of chromosome Y after gender-mismatched transplantation of male PSC into female rats. Transplanted PSC displayed long-lasting survival, whereas muscle fibroblasts were unable to integrate into the host liver. The differentiation potential of PSC was further verified by the transplantation of clonally expanded PSC. PSC clones maintained the expression of stellate cell and stem cell markers and preserved their differentiation potential, which indicated self-renewal potential of PSC. These findings demonstrate that PSC have stem cell characteristics and can contribute to the regeneration of injured organs through differentiation across tissue boundaries.
Late Onset Poststroke Seizures  [cached]
Ba?ak Karakurum G?KSEL,Mehmet KARATA?,Meliha TAN,,Tülin YILDIRIM
Journal of Neurological Sciences , 2005,
Abstract: The most common cause of seizures is cerebrovascular disease in elderly population. Late onset seizures are not investigated as well as early onset seizures in patients with stroke. There is no common consensus about clinical, electrophysiological and radiological features of these seizures. In this study, 55 patients with late onset seizure who had stroke history were investigated. The 49 % of patients were women, the mean ages of patients were 63.9±9.2 years. The mean of duration between stroke and the first seizure was 30.4±36.8 months and the mean of following time was 14±13 months. The 89% of patients ischemic stroke and 11% of patients had hemorrhagic stroke. The lesion localizations were cortical in 17 (30.9%) patients, subcortical in 8 (14.5%) and cortico-subcortical in 29 (52.7%). As a result 84 % patients’ lesions were cortical localization. There were partial seizure in 39 (%70.9) patients, generalized tonic-clonic seizure in 16 (29.1%) patients. 43 (78%) patients had no seizure during antiepileptic therapy. 7 (12.7%) patients had seizure after beginning antiepileptic drug due to stopping drug, low blood level of drug and ineffectiveness of drug. 5 (9%) patients had not been given drug because of first seizure and no seizure during follow-up. In conclusion, the late onset poststroke seizures seem frequently in ischemic stroke, the reccurence rate was high and partial type seizures were more common than generalized and cortical localization was seen frequently. On the other hand, this condition has good prognosis.
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