Producción simbólica en tiempos de globalización

162 p.Las investigaciones que tratan sobre Globalización generalmente tratan de abordar la complejidad del fenómeno a partir de la necesaria interdisciplinariedad que reclama el objeto para su aprehensión, sobre la base del reconocimiento de la complementariedad de los conocimientos desarrollados por las Ciencias Sociales y la Humanidades. Sin embargo, esto no permite negar la trayectoria intelectual y los intereses de los investigadores, los cuales en cierta medida permiten comprender los criterios que justifi can la preferencia de determinados enfoques considerados adecuados para afrontar una realidad cuya multiplicidad de aristas puede sobrepasar al observador más dedicado.Agradecimientos 5 Presentación 7 Introducción 11 Primera parte: Producción Simbólica y Globalzación I. Antecedentes y Planteamiento de una problemática 17 I.1) La Sociología y los estudios culturales en la Globalización 17 I.2) Transformaciones tecnológicas y la producción de cultura. 22 I.3) Producción musical y su institucionalidad: La Sociedad Chilena del Derecho de Autor. 25 II. Producción Simbólica y Globalización: un acercamiento teórico 33 II.1) La emergencia de la pregunta por la cultura: la Teoría del Conocimiento. 35 II.2) De la antropologización a la ontologización: el Proyecto Fenomenológico 44 II.3) Habla como discurso, lenguaje como sistema: el Estructuralismo. 52 II.4) ¿Cómo pensar lo simbólico desde el punto de vista sociológico?: el Poder y las Condiciones Sociales de Signifi cación. 62 II.5) Producción de sentido y Globalización: Hibridación, Mestizaje y Mediación en la construcción de Hegemonía. 71 II.6) Algunas correspondencias entre Música y Producción Simbólica. 77 II.7) Alcances del concepto de Producción Simbólica. 80 Segunda parte: Percepción de los mísicos miembros de la Sociedad Chilena del Derecho de Autor respecto a la Producción Simbólica en contexto de Globalización I. Aspectos generales del estudio. 85 I.1) Pregunta de Investigación. 85 I.2) Objetivos del Estudio. 85 I.3) Hipótesis generales de la investigación. 86 simón palominos, elías f 162 arías y gonzalo utreras II. Análisis de los datos recogidos en el estudio. 88 II.1) Autopercepción de la producción musical de los miembros de la SCD. 88 II.2) Autopercepción de las relaciones de poder simbólico en la producción musical de los miembros de la SCD. 92 II.3) Percepción de la función de la SCD en el desarrollo de la producción simbólica. 96 II.4) Percepción de los miembros de la SCD en relación con la Industria Cultural. 99 II.5) Percepción de los miembros de la SCD en relación con el Estado. 103 II.6) Percepción de los miembros de la SCD en relación con las Audiencias. 109 II.7) Percepción de los miembros de la SCD en relación con las Tecnologías de la Información y las Comunicaciones (TIC’s). 114 II.8) Percepción de la Función Mediadora de la SCD. 121 II.9) Modelo Accional (Actancial) de la Producción Simbólica en el contexto de la Globalización. 126 III. Conclusiones del Estudio. 130 Anexo metodológico I. Universo y Diseño Muestral. 141 II. Técnica de recolección de datos 143 III. Construcción del Instrumento. 145 IV. Instrumento. 148 Bibliografía 15

Role of PPAR γ in the differentiation and function of neurons

© 2014 Rodrigo A. Quintanilla et al.Neuronal processes (neurites and axons) have an important role in brain cells communication and, generally, they are damaged in neurodegenerative diseases. Recent evidence has showed that the activation of PPARγ pathway promoted neuronal differentiation and axon polarity. In addition, activation of PPARγ using thiazolidinediones (TZDs) prevented neurodegeneration by reducing neuronal death, improving mitochondrial function, and decreasing neuroinflammation in neuropathic pain. In this review, we will discuss important evidence that supports a possible role of PPARγ in neuronal development, improvement of neuronal health, and pain signaling. Therefore, activation of PPARγ is a potential target with therapeutic applications against neurodegenerative disorders, brain injury, and pain regulation

TNF-alpha increases production of reactive oxygen species through Cdk5 activation in nociceptive neurons

The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH oxidase has been documented during inflammatory pain. However, the molecular mechanism involved in their activation is not fully understood. We reported earlier a key role of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we demonstrated that TNF-alpha increased p35 expression, a Cdk5 activator, causing Cdk5-mediated TRPV1 phosphorylation followed by an increment in Ca2+ influx in nociceptive neurons and increased pain sensation. Here we evaluated if Cdk5 activation mediated by p35 transfection in HEK293 cells or by TNF-alpha treatment in primary culture of nociceptive neurons could increase ROS production. By immunofluorescence we detected the expression of catalytic subunit (Nox1 and Nox2) and their cytosolic regulators (NOXO1 and p47(phox)) of NOX1 and NOX2/NADPH oxidase complexes, and their co-localization with Cdk5/p35 in HEK293 cells and in nociceptive neurons. By using a hydrogen peroxide sensor, we detected a significant increase of ROS production in p35 transfected HEK293 cells as compared with control cells. This effect was significantly blocked by VAS2870 (NADPH oxidase inhibitor) or by roscovitine (Cdk5 activity inhibitor). Also by using another ROS probe named DCFH-DA, we found a significant increase of ROS production in nociceptive neurons treated with TNF-a and this effect was also blocked by VAS2870 or by roscovitine treatment. Interestingly, TNF-alpha increased immunodetection of p35 protein and NOX1 and NOX2/NADPH oxidase complexes in primary culture of trigeminal ganglia neurons. Finally, the cytosolic regulator NOXO1 was significantly translocated to plasma membrane after TNF-alpha treatment and roscovitine blocked this effect. Altogether these results suggest that Cdk5 activation is implicated in the ROS production by NOX1 and NOX2/NADPH oxidase complexes during inflammatory pain.FONDECYT 1140325 1151043 FONDAP 1515001

TNF-α Increases Production of Reactive Oxygen Species through Cdk5 Activation in Nociceptive Neurons

The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH oxidase has been documented during inflammatory pain. However, the molecular mechanism involved in their activation is not fully understood. We reported earlier a key role of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we demonstrated that TNF-α increased p35 expression, a Cdk5 activator, causing Cdk5-mediated TRPV1 phosphorylation followed by an increment in Ca2+ influx in nociceptive neurons and increased pain sensation. Here we evaluated if Cdk5 activation mediated by p35 transfection in HEK293 cells or by TNF-α treatment in primary culture of nociceptive neurons could increase ROS production. By immunofluorescence we detected the expression of catalytic subunit (Nox1 and Nox2) and their cytosolic regulators (NOXO1 and p47phox) of NOX1 and NOX2/NADPH oxidase complexes, and their co-localization with Cdk5/p35 in HEK293 cells and in nociceptive neurons. By using a hydrogen peroxide sensor, we detected a significant increase of ROS production in p35 transfected HEK293 cells as compared with control cells. This effect was significantly blocked by VAS2870 (NADPH oxidase inhibitor) or by roscovitine (Cdk5 activity inhibitor). Also by using another ROS probe named DCFH-DA, we found a significant increase of ROS production in nociceptive neurons treated with TNF-α and this effect was also blocked by VAS2870 or by roscovitine treatment. Interestingly, TNF-α increased immunodetection of p35 protein and NOX1 and NOX2/NADPH oxidase complexes in primary culture of trigeminal ganglia neurons. Finally, the cytosolic regulator NOXO1 was significantly translocated to plasma membrane after TNF-α treatment and roscovitine blocked this effect. Altogether these results suggest that Cdk5 activation is implicated in the ROS production by NOX1 and NOX2/NADPH oxidase complexes during inflammatory pain

Cdk5 regulates Rap1 activity

Rap1 signaling is important for migration, differentiation, axonal growth, and during neuronal polarity. Rap1 can be activated by external stimuli, which in turn regulates specific guanine nucleotide exchange factors such as C3G, among others. Cdk5 functions are also important to neuronal migration and differentiation. Since we found that pharmacological inhibition of Cdk5 by using roscovitine reduced Rap1 protein levels in COS-7 cells and also C3G contains three putative phosphorylation sites for Cdk5, we examined whether the Cdk5-dependent phosphorylation of C3G could affect Rap1 expression and activity. We co-transfected C3G and tet-OFF system for p35 over-expression, an activator of Cdk5 activity into COS-7 cells, and then we evaluated phosphorylation in serine residues in C3G by immunoprecipitation and Western blot. We found that p35 over-expression increased C3G-serine-phosphorylation while inhibition of p35 expression by tetracycline or inhibition of Cdk5 activity with roscovit

Prenatal stress down-regulates Reelin expression by methylation of its promoter and induces adult behavioral impairments in rats.

Prenatal stress causes predisposition to cognitive and emotional disturbances and is a risk factor towards the development of neuropsychiatric conditions like depression, bipolar disorders and schizophrenia. The extracellular protein Reelin, expressed by Cajal-Retzius cells during cortical development, plays critical roles on cortical lamination and synaptic maturation, and its deregulation has been associated with maladaptive conditions. In the present study, we address the effect of prenatal restraint stress (PNS) upon Reelin expression and signaling in pregnant rats during the last 10 days of pregnancy. Animals from one group, including control and PNS exposed fetuses, were sacrificed and analyzed using immunohistochemical, biochemical, cell biology and molecular biology approaches. We scored changes in the expression of Reelin, its signaling pathway and in the methylation of its promoter. A second group included control and PNS exposed animals maintained until young adulthood for behavioral studies. Using the optical dissector, we show decreased numbers of Reelin-positive neurons in cortical layer I of PNS exposed animals. In addition, neurons from PNS exposed animals display decreased Reelin expression that is paralleled by changes in components of the Reelin-signaling cascade, both in vivo and in vitro. Furthermore, PNS induced changes in the DNA methylation levels of the Reelin promoter in culture and in histological samples. PNS adult rats display excessive spontaneous locomotor activity, high anxiety levels and problems of learning and memory consolidation. No significant visuo-spatial memory impairment was detected on the Morris water maze. These results highlight the effects of prenatal stress on the Cajal-Retzius neuronal population, and the persistence of behavioral consequences using this treatment in adults, thereby supporting a relevant role of PNS in the genesis of neuropsychiatric diseases. We also propose an in vitro model that can yield new insights on the molecular mechanisms behind the effects of prenatal stress

Microtubule-associated protein 1B interaction with tubulin tyrosine ligase contributes to the control of microtubule tyrosination

Microtubule-associated protein 1B (MAP1B) is the first microtubule-associated protein to be expressed during nervous system development. MAP1B belongs to a large family of proteins that contribute to the stabilization and/or enhancement of microtubule polymerization. These functions are related to the control of the dynamic properties of microtubules. The C-terminal domain of the neuronal α-tubulin isotype is characterized by the presence of an acidic polypeptide, with the last amino acid being tyrosine. This tyrosine residue may be enzymatically removed from the protein by an unknown carboxypeptidase activity. Subsequently, the tyrosine residue is again incorporated into this tubulinby another enzyme, tubulin tyrosine ligase, to yield tyrosinated tubulin. Because neurons lacking MAP1B have a reduced proportion of tyrosinated microtubules, we analyzed the possible interaction between MAP1B and tubulin tyrosine ligase. Our results show that these proteins indeed interact and that the interaction is not affected by MAP1B phosphorylation. Additionally, neurons lacking MAP1B, when exposed to drugs that reversibly depolymerize microtubules, do not fully recover tyrosinated microtubules upon drug removal. These results suggest that MAP1B regulates tyrosination of α-tubulin in neuronal microtubules. This regulation may be important for general processes involved in nervous system development such as axonal guidance and neuronal migration.This work was supported by grants from DID I03/02-2, Fundacion Andes C1406012, Fondecyt 1060040 and CSIC 21 05/06 to C.G.-B., Fondecyt to R.B.M., and by grants from the Spanish Ministry of Education and Science, and Ministry of Health to J.A.Peer reviewe

Microtubule-associated protein 1B interaction with tubulin tyrosine ligase contributes to the control of microtubule tyrosination

Microtubule-associated protein 1B (MAP1B) is the first microtubule- associated protein to be expressed during nervous system development. MAP1B belongs to a large family of proteins that contribute to the stabilization and/or enhancement of microtubule polymerization. These functions are related to the control of the dynamic properties of microtubules. The C-terminal domain of the neuronal α-tubulin isotype is characterized by the presence of an acidic polypeptide, with the last amino acid being tyrosine. This tyrosine residue may be enzymatically removed from the protein by an unknown carboxypeptidase activity. Subsequently, the tyrosine residue is again incorporated into this tubulinby another enzyme, tubulin tyrosine ligase, to yield tyrosinated tubulin. Because neurons lacking MAP1B have a reduced proportion of tyrosinated microtubules, we analyzed the possible interaction between MAP1B and tubulin tyrosine ligase. Our results show that these proteins indeed interact and that the