On The Delays In Spiking Neural P Systems

In this work we extend and improve the results done in a previous work on simulating Spiking Neural P systems (SNP systems in short) with delays using SNP systems without delays. We simulate the former with the latter over sequential, iteration, join, and split routing. Our results provide constructions so that both systems halt at exactly the same time, start with only one spike, and produce the same number of spikes to the environment after halting.Comment: Presented at the 6th Symposium on the Mathematical Aspects of Computer Science (SMACS2012), Boracay, Philippines. 6 figures, 6 pages, 2 column

Muscarinic Receptors, from Synaptic Plasticity to its Role in Network Activity

Acetylcholine acting via metabotropic receptors plays a key role in learning and memory by regulating synaptic plasticity and circuit activity. However, a recent overall view of the effects of muscarinic acetylcholine receptors (mAChRs) on excitatory and inhibitory long-term synaptic plasticity and on circuit activity is lacking. This review focusses on specific aspects of the regulation of synaptic plasticity and circuit activity by mAChRs in the hippocampus and cortex. Acetylcholine increases the excitability of pyramidal neurons, facilitating the generation of dendritic Ca2+-spikes, NMDA-spikes and action potential bursts which provide the main source of Ca2+ influx necessary to induce synaptic plasticity. The activation of mAChRs induced Ca2+ release from intracellular IP3-sensitive stores is a major player in the induction of a NMDA independent long-term potentiation (LTP) caused by an increased expression of AMPA receptors in hippocampal pyramidal neuron dendritic spines. In the neocortex, activation of mAChRs also induces a long-term enhancement of excitatory postsynaptic currents. In addition to effects on excitatory synapses, a single brief activation of mAChRs together with short repeated membrane depolarization can induce a long-term enhancement of GABA A type (GABAA) inhibition through an increased expression of GABAA receptors in hippocampal pyramidal neurons. By contrast, a long term depression of GABAA inhibition (iLTD) is induced by muscarinic receptor activation in the absence of postsynaptic depolarizations. This iLTD is caused by an endocannabinoid-mediated presynaptic inhibition that reduces the GABA release probability at the terminals of inhibitory interneurons. This bidirectional long-term plasticity of inhibition may dynamically regulate the excitatory/inhibitory balance depending on the quiescent or active state of the postsynaptic pyramidal neurons. Therefore, acetylcholine can induce varied effects on neuronal activity and circuit behavior that can enhance sensory detection and processing through the modification of circuit activity leading to learning, memory and behaviorThis work was supported by the following Grants: BFU2016-80802-P AEI/FEDER, UE to D. Fernández de Sevilla, SAF2016-7642 AEI/FEDER, UE to A. Núñez and BFU2005-07486 to W. Buñ

Acetylcholine facilitates a depolarization-induced enhancement of inhibition in rat CA1 pyramidal neurons

Cholinergic mechanisms in the hippocampus regulate forms of synaptic plasticity linked with cognition and spatial navigation, but the underlying mechanisms remain largely unknown. Here, in rat hippocampal CA1 pyramidal cells under blockade of ionotropic glutamate receptors, we report that a single acetylcholine pulse and repeated depolarization activated a robust and enduring postsynaptic depolarization-induced enhancement of inhibition (DEI) that masked a presynaptic depolarization-induced suppression of inhibition (DSI). Increased cytosolic Ca2+ and M1-muscarinic receptor activation caused the rise in voltage-sensitive α5βγ2-containing γ-aminobutyric acid type-A receptors that generated DEI. In summary, this muscarinic-mediated activity-dependent plasticity rapidly transfers depolarization effects on inhibition from presynaptic suppression or DSI to postsynaptic enhancement or DEI, a change potentially relevant in behaviorThis work was supported by Ministerio de Ciencia y Tecnología, BFU2005-07486 and Comunidad Autónoma de Madrid, GR/SAL/ 0877/2004 grants to W.B., and Ministerio de Ciencia y Tecnología, BFU2008-03488, BFU2011-23522, and BFU2013-43668P grants to D.F.d.S. S.D. was a doctoral fellow at the Instituto Cajal supported by grant (BFU2005-07486) and is now a postdoctoral fellow in the team “Synaptic Plasticity and Neural Networks” at Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8118, Université Paris Descartes, France. D.F.d.S was supported by a Ramón y Cajal Contract and is now a Professor at the “Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, Universidad Autónoma de Madrid

Near and far field models of external fluid mechanics of Ocean Thermal Energy Conversion (OTEC) power plants

Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Civil and Environmental Engineering, 2013.Cataloged from PDF version of thesis.Includes bibliographical references (p. 126-130).The world is facing the challenge of finding new renewable sources of energy - first, in response to fossil fuel reserve depletion, and second, to reduce greenhouse gas emissions. Ocean Thermal Energy Conversion (OTEC) can provide renewable energy by making use of the temperature difference between the surface ocean and deep ocean water in a Rankine cycle. An OTEC plant pumps huge volumes of water from the surface and nearly 1 km depth, and releases it at an intermediate depth. The effects of this enormous flux are crucial to understand since disruption of the ambient temperature stratification can affect the efficiency of the plant itself and of adjacent plants. This thesis aims to study the external fluid mechanics of offshore OTEC power plants, to assess their environmental impact and to help analyze whether OTEC plants can provide a sustainable source of energy. Although there has been interest in OTEC for several decades, so far primarily physical and analytical models have been developed. In this study numerical models are developed to model OTEC operating plants: integral models for the near and intermediate field and a large-scale ocean general circulation model. Two strategies in modeling OTEC plant discharge are used to analyze plume dynamics: the "Brute Force" approach, in which a circulation model, MITgcm, computes the near, intermediate and far field mixing; and the "Distributed Sources and Sinks" approach, in which the near and intermediate field are represented in the circulation model by sources and sinks of mass computed by integral models. This study concludes that the Brute Force modeling strategy is highly computationally demanding and sometimes inaccurate. Such simulations are very sensitive to model resolution and may require the use of unrealistic model parameters. The Distributed Sources and Sinks approach was found to be capable of modeling the plume dynamics accurately. This method can be applied to the study of adjacent OTEC power plant interaction, redistribution of nutrients, and propagation of contaminants.by Mariana Rodríguez Buño.S.M

Cholinergic-mediated IP3-ereceptor activation induces long-lasting synaptic enhancement in CA1 pyramidal neurons

Cholinergic–glutamatergic interactions influence forms of synaptic plasticity that are thought to mediate memory and learning. We tested in vitro the induction of long-lasting synaptic enhancement at Schaffer collaterals by acetylcholine (ACh) at the apical dendrite of CA1 pyramidal neurons and in vivo by stimulation of cholinergic afferents. In vitro ACh induced a Ca2+ wave and synaptic enhancement mediated by insertion of AMPA receptors in spines. Activation of muscarinic ACh receptors (mAChRs) and Ca2+ release from inositol 1,4,5-trisphosphate (IP3)-sensitive stores were required for this synaptic enhancement that was insensitive to blockade of NMDA receptors and also triggered by IP3 uncaging. Activation of cholinergic afferents in vivo induced an analogous atropine-sensitive synaptic enhancement. We describe a novel form of synaptic enhancement (LTPIP3) that is induced in vitro and in vivo by activation of mAChRs. We conclude that Ca2+ released from postsynaptic endoplasmic reticulum stores is the critical event in the induction of this unique form of long-lasting synaptic enhancement

Maloclusión en niños en edad escolar : análisis de los factores de riesgo

Investigadores responsables: Ramón Álvarez-Vaz, Graciela Buño, María Noel Mesa, Laura Nalbarte, María Eugenia Riaño.Presentación de la colección. -- I Metodología. 1. Introducción 1.1. Objetivos. 1.2. Antecedentes de estudios sobre maloclusión. -- 2. Marco Teórico. 2.1. Factores genéticos. 2.2. Factores ambientales. 2.3. Papel del ortodoncista . -- 3. Materiales y métodos. 3.1. Material utilizado. 3.2. Metodología de trabajo. -- II Resultados 4. Análisis previo de la información. 4.1. Descripción general de la base. 4.2. Construcción de la variable estado nutricional. 4.3. Variables del bloque de mordida cruzada. 4.4. Análisis de consistencia de los datos. 4.4.1. Mordida abierta. 4.4.2. Mordida cruzada. 4.4.3. Diastemas y apiñamientos. 4.5. Reconstrucción del grado de severidad. -- 5. Cálculo de los pesos de los individuos. -- 6. Análisis de las variables por bloque. 6.1. Características orofaciales. 6.2. Hábitos 6.3. Espacios y dimensiones. 6.4. Mordida abierta. 6.5. Mordida cruzada . 6.6. Conclusiones. -- 7. Análisis de grupos. -- 7.1. Determinación del número de grupos. 7.2. Análisis y descripción de los grupos. 7.2.1. Grupo 1: Individuos con presencia de mordida abierta. 7.2.2. Grupo 2: Individuos con maloclusiones asociadas al bloque de mordida cruzada. 7.2.3. Grupo 3: Individuos con maloclusiones asociadas al resalte y al sobrepase. -- 8. Construcción de un algoritmo predictivo de clasificación. 8.1. Resultados obtenidos. -- 9. Conclusiones. -- III Apéndices

Heterosynaptic metaplastic regulation of synaptic efficacy in CA1 pyramidal neurons of rat hippocampus

International audienceThe induction threshold, and the magnitude and direction of changes in synaptic plasticity may depend on the previous history of neuronal activity. This phenomenon, termed "metaplasticity," could play an important role in integration processes by coordinating the modulation of synapses. Although metaplasticity has been analyzed extensively, its underlying cellular mechanisms remain largely unknown. Using in vitro electrophysiological and computer simulation approaches, we investigated the contribution of the slow Ca 2؉-dependent afterhyperpolariza-tion (sAHP) in the metaplastic control of the induction of long-term potentiation (LTP) at convergent CA3-CA1 pyramidal neuron synapses. We report that classical conditioning protocols may lead to the simultaneous induction of a sustained homosynaptic LTP and a potentiation of the sAHP that endured Ϸ1 h. The sAHP potentiation dramatically altered the spike responses of the CA1 pyramidal neuron. Of particular interest was the reduction of the CA1 neuron excitability and, consequently, of the capacity of a nonpotentiated synaptic input to elicit spikes while the sAHP was potentiated. This reduction in excitability temporarily prevented nonpotentiated synaptic inputs to exhibit an LTP induced by presynaptic tetanization. This metaplasticity was strongly resistant to increases in the magnitude of synaptic tetanization protocols. We propose that this het-erosynaptic metaplasticity, mediated by intrinsic cellular mechanisms, triggered by brief periods of activity, and relying on changes of a slow Ca 2؉-activated K ؉ current, may contribute to adjusting the efficacy of synaptic connections and shaping network behavior to regulate integration processes

Bidirectional hebbian plasticity induced by low-frequency stimulationin basal dendrites of rat barrel cortex layer 5 pyramidal neurons

According to Hebb’s original hypothesis (Hebb,1949), synapses are reinforced when presynaptic activity triggers postsynaptic firing, resulting in long-term potentiation (LTP) of synaptic efficacy. Long-term depression (LTD) is a use-dependent decrease in synaptic strength that is thought to be due to synaptic in put causing a weak postsynaptic effect. Although the mechanisms that mediate long-term synaptic plasticity have been investigated for at least three decades not all question have as yet been answered. Therefore, we aimed at determining the mechanisms that generate LTP or LTD with the simplest possible protocol Low-frequency stimulation of basal dendrite inputs in Layer 5 pyramidal neurons of the rat barrel cortex induces LTP. This stimulation triggered an EPSP, an action potential (AP) burst, and a Ca2+ spike. The same stimulation induced LTD following manipulations that reduced the Ca2+ spike and Ca2+ signal or the AP burst. Low-frequency whisker deflections induced similar bidirectional plasticity of action potential evoked responses in anesthetized rats. These results suggest that both in vitro and in vivo similar mechanisms regulate the balance between LTP and LTD. This simple induction form of bidirectional hebbian plasticity could be present in the natural conditions to regulate the detection, flow, and storage of sensorimotor informationWork supported by “Ministerio de Ciencia y Tecnología y Ministerio de Ciencia e Innovación” grants (BFU2005-07486, BFU2008-03488, SAF2009-10339, BFU2011-23522, BFU2012-36107, BFU2013-43668-P and BFU2016-80802-P) and a “Comunidad Autónoma de Madrid” (GR/SAL/0877/2004) grant. Dr .D. Fernández de Sevilla was a post doctoral fellow at the “Instituto Cajal,” funded by GR/SAL/0877/2004 and a “Ministerio de Ciencia and Tecnología” grant (BFU2005-07486).He was subsequently supported by a Ramón y Cajal Contract and is now a Professor at the “Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, Universidad Autónoma de Madrid.” Dr. Andrea Diez was a doctoral fellow funded by the BFU2011-23522 grant and is now a post doctoral fellow funded by “Ministerio de Ciencia e Innovación” grant (BFU2013- 43741-P) at the “Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, Universidad Autónoma de Madrid.” N. Barros-Zulaica was a doctoral fellow funded by the BFU2012-36107 gran