La renovación de la palabra en el bicentenario de la Argentina : los colores de la mirada lingüística

El libro reúne trabajos en los que se exponen resultados de investigaciones presentadas por investigadores de Argentina, Chile, Brasil, España, Italia y Alemania en el XII Congreso de la Sociedad Argentina de Lingüística (SAL), Bicentenario: la renovación de la palabra, realizado en Mendoza, Argentina, entre el 6 y el 9 de abril de 2010. Las temáticas abordadas en los 167 capítulos muestran las grandes líneas de investigación que se desarrollan fundamentalmente en nuestro país, pero también en los otros países mencionados arriba, y señalan además las áreas que recién se inician, con poca tradición en nuestro país y que deberían fomentarse. Los trabajos aquí publicados se enmarcan dentro de las siguientes disciplinas y/o campos de investigación: Fonología, Sintaxis, Semántica y Pragmática, Lingüística Cognitiva, Análisis del Discurso, Psicolingüística, Adquisición de la Lengua, Sociolingüística y Dialectología, Didáctica de la lengua, Lingüística Aplicada, Lingüística Computacional, Historia de la Lengua y la Lingüística, Lenguas Aborígenes, Filosofía del Lenguaje, Lexicología y Terminología

Redox control of brain calcium in health and disease

Calcium ion is a highly versatile cellular messenger. Calcium signals-defined as transient increments in intracellular-free calcium concentration-elicit a multiplicity of responses that depend on cell type and signal properties such as their intensity, duration, cellular localization, and frequency. The vast literature available on the role of calcium signals in brain cells, chiefly centered on neuronal cells, indicates that calcium signals regulate essential neuronal functions, including synaptic transmission, gene expression, synaptic plasticity processes underlying learning and memory, and survival or death. The eight articles comprising this forum issue address different and novel aspects of calcium signaling in normal neuronal function, including how calcium signals interact with the generation of reactive species of oxygen/nitrogen with various functional consequences, and focus also on how abnormal calcium homeostasis and signaling, plus oxidative stress, affect overall brain p

Inositol trisphosphate and excitation-contraction coupling in skeletal muscle

The role of inositol trisphosphate as a chemical messenger in excitation-contraction coupling is discussed, both in terms of positive and negative results. The evidence presented includes experiments on the effect of inositol trisphosphate in intact and skinned fibers, in calcium release from isolated sarcoplasmic reticulum vesicles, in activation of single calcium release channels incorporated in planar bilayers, and biochemical experiments that have established the presence of all the intermediate steps involved in the metabolism of phosphoinositides, both in intact muscle and in isolated membranes. From these results, it is clear that a role for inositol triphosphate in skeletal muscle function is highly likely; whether this molecule is the physiological messenger in excitation-contraction coupling remains to be established. © 1989 Plenum Publishing Corporation

Sodium-calcium exchange in transverse tubules isolated from frog skeletal muscle

Transverse tubule vesicles isolated from frog skeletal muscle display sodium-calcium exchange activity, which was characterized measuring 45Ca influx in vesicles incubated with sodium. The initial rates of exchange varied as a function of the membrane diffusion potentials imposed across the membrane vesicles, increasing with positive intravesicular potentials according to an electrogenic exchange with a stoichiometry greater than 2 sodium ions per calcium ion transported. The exchange activity was a saturable function of extravesicular free calcium, with an apparent K0.5 value of 3 μM and maximal rates of exchange ranging from 3 to 5 nmol/mg protein per 5 s. The exchange rate increased when intravesicular sodium concentration was increased; saturation was approached when vesicles were incubated with concentrations of 160 mM sodium. The isolated transverse tubule vesicles, which are sealed with the cytoplasmic side out, had a luminal content of 112±39 nmol calcium per mg protein. In th

Sodium transport inhibition by selective mitochondrial inhibitors in the urinary bladder of the toad

The effects of selective mitochondrial inhibitors on the short‐circuit current and oxygen consumption displayed by the isolated urinary bladder of the toad was studied. Three types of compounds were used: (a) electron transfer inhibitors, Amytal, Cyanide and Antimycin A; (b) energy transfer inhibitors Guanidine, Oligomycin and Rutamycin; and (c) uncoupling agents, Carbonyl cyanide m‐chlorophenylhydrazone and 2–4 dinitrophenol. The kinetics of inhibition of oxygen consumption indicated that the inhibitors tested were effectively reaching the mitochondria of the bladder cells. Different kinetics of inhibition of short‐circuit current were obtained with the various inhibitors tested. Uncouplers and electron transfer inhibitors rapidly blocked the short‐circuit current; energy transfer inhibitors only produced a slow and partial inhibition. A site of energy‐coupling, tentatively identified with the intermediate formed in the energy transfer reactions closest to the electron transfer chain

Calcium, iron and neuronal function

Publicación ISICalcium and iron play dual roles in neuronal function: they are both essential but when present in excess they cause neuronal damage and may even induce neuronal death. Calcium signals are required for synaptic plasticity, a neuronal process that entails gene expression and which is presumably the cellular counterpart of cognitive brain functions such as learning and memory. Neuronal activity generates cytoplasmic and nuclear calcium signals that in turn stimulate pathways that promote the transcription of genes known to participate in synaptic plasticity. In addition, evidence discussed in this article shows that iron deficiency causes learning and memory impairments that persist following iron repletion, indicating that iron is necessary for normal development of cognitive functions. Recent results from our group indicate that iron is required for long-term potentiation in hippocampal CA1 neurons and that iron stimulates ryanodine receptor-mediated calcium release through ROS produced via the Fenton reaction leading to stimulation of the ERK signaling pathway. These combined results support a coordinated action between iron and calcium in synaptic plasticity and raise the possibility that elevated iron levels may contribute to neuronal degeneration through excessive intracellular calcium increase caused by iron-induced oxidative stress

Crosstalk between calcium and redox signaling: From molecular mechanisms to health implications

Studies done many years ago established unequivocally the key role of calcium as a universal second messenger. In contrast, the second messenger roles of reactive oxygen and nitrogen species have emerged only recently. Therefore, their contributions to physiological cell signaling pathways have not yet become universally accepted, and many biological researchers still regard them only as cellular noxious agents. Furthermore, it is becoming increasingly apparent that there are significant interactions between calcium and redox species, and that these interactions modify a variety of proteins that participate in signaling transduction pathways and in other fundamental cellular functions that determine cell life or death. This review article addresses first the central aspects of calcium and redox signaling pathways in animal cells, and continues with the molecular mechanisms that underlie crosstalk between calcium and redox signals under a number of physiological or pathological conditi

Phospholipase C activity in membranes and a soluble fraction isolated from frog skeletal muscle

Highly purified triads and transverse tubules, as well as a soluble fraction isolated from frog skeletal muscle, hydrolyze exogenous phosphatidylinositol 4,5-bisphosphate forming inositol 1,4,5-trisphosphate with maximal rates in the range 0.5-1 nmol/mg per min at pCa 3. Sarcoplasmic reticulum membranes present a minor activity. The hydrolysis rates in triads were 0.072 ± 0.015 nmol/mg per min at pCa 7, increasing to 0.263 ± 0.026 nmol/mg per min at pCa 5 with 1.0 mM Mg and 0.1 mM substrate. The phospholipase C activity of isolated transverse tubules at pCa 3 was 0.570 ± 0.032 nmol/mg per min. Since triads contain 10% transverse tubules, and correcting for the small contribution of sarcoplasmic reticulum, the calculated phospholipase C activity of transverse tubules at pCa 3 is about 10-times higher than the observed values, suggesting loss of activity during isolation. The activation by calcium was also observed in a soluble fraction and was neither replaced nor inhibited by magnesiu

Mecp2 mediates experience-dependent transcriptional upregulation of ryanodine receptor type-3

Mecp2 is a DNA methylation reader that plays a critical role in experience-dependent plasticity. Increasing evidence supports a role for epigenetic modifications in activity-induced gene expression. Hence, candidate genes related to such phenomena are of great interest. Ryanodine receptors are intracellular calcium channels that contribute to hippocampal synaptic plasticity, dendritic spine remodeling, and participate in learning and memory processes. Here we exposed mice to the enriched environment (EE) paradigm, which through increased stimulation induces experience dependent-plasticity, to explore a role for methyl-cytosines, and Mecp2 in directing Ryanodine receptor 3 (Ryr3) transcriptional activity. EE induced a hippocampal-specific increase in the methylation of discrete cytosines located at a Ryr3 isoform promoter; chromatin immunoprecipitation experiments revealed that EE increased Mecp2 binding to this Ryr3 isoform promoter. Interestingly, the experimental paradigm induced robust Ryr3 upregulation, accompanied by miR132-dependent suppression of p250GAP, a pathway driving synaptogenesis. In contrast to WT mice, Mecp2-null mice showed diminished levels of Ryr3 and displayed impaired EE-induced Ryr3 upregulation, compromising miR132 dependent suppression of p250GAP and experience-dependent structural plasticity. Based on these results, we propose that Mecp2 acts as a transcriptional activator of Ryr3, contributing to experience- dependent plasticity.Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT), 1140162, 1140545 / Biomedical Neuroscience Institute, BNI P-09-015F Chilean Government through the Centers of Excellence Basal Financing Program of CONICY