16 resultados para synaptic learning mechanisms

em Aston University Research Archive


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This paper argues that it is possible to identify factors which pre-dispose organizations to adopt effective learning strategies and processes. It is hypothesized that effective OL is associated with: profitability, environmental uncertainty, structure, approach to HRM and quality orientation. The study focuses on forty-four manufacturing organizations, and draws on longitudinal data gathered through interviews. The findings suggest that two of these variables - approach to HRM and quality orientation - are particularly strongly correlated with measures of OL. It is concluded that effective learning mechanisms, with the potential to improve the quality of OL processes, are more likely to be established in businesses where HRM and quality initiatives are well established.

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The national systems of innovation (NIS) approach focuses on the patterns and the determinants of innovation processes from the perspective of nation-states. This paper reports on continuing work on the application of an NIS model to the development of technological capability in Turkey. Initial assessment of the literature shows that there are a number of alternative conceptualisations of NIS. An attempt by the Government to identify a NIS for Turkey shows the main actors in the system but does not pay sufficient attention to the processes of interactions between agents within the system. An operational model should be capable of representing these processes and interactions and assessing the strengths and weaknesses of the NIS. For industrialising countries, it is also necessary to incorporate learning mechanisms into the model. Further, there are different levels of innovation and capability in different sectors which the national perspective may not reflect. This paper is arranged into three sections. The first briefly explains the basics of the national innovation and learning system. Although there is no single accepted definition of NIS, alternative definitions reviewed share some common characteristics. In the second section, an NIS model is applied to Turkey in order to identify the elements, which characterise the country’s NIS. This section explains knowledge flow and defines the relations between the actors within the system. The final section draws on the “from imitation to innovation” model apparently so successful in East Asia and assesses its applicability to Turkey. In assessing Turkey’s NIS, the focus is on the automotive and textile sectors.

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This edited book is intended for use by students, academics and practitioners who take interest in the outsourcing and offshoring of information technology and business services and processes. The book offers a review of the key topics in outsourcing and offshoring, populated with practical frameworks that serve as a tool kit for practitioners, academics and students. The range of topics covered in this book is wide and diverse, and represents both client and supplier perspectives on sourcing of global services. Various aspects related to the decision making process (e.g., asset transfer), learning mechanisms and organizational practices for managing outsourcing relationships are discussed in great depth. Contemporary sourcing models, including cloud services, are examined. Client dependency on the outsourcing provider, and social aspects, such as identity, are discussed in detail. Furthermore, resistance in outsourcing and failures are investigated to derive lessons as to how to avoid them and improve efficiency in outsourcing. Topics discussed in this book combine theoretical and practical insights regarding challenges that both clients and vendors face. Case studies from client and vendor organizations are used extensively throughout the book. Last but not least, the book examines current and future trends in outsourcing and offshoring, placing particular attention on the centrality of innovation in sourcing arrangements, and how innovation can be realized in outsourcing. The book is based on a vast empirical base brought together through years of extensive research by leading researchers in information systems, strategic management and operations.

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This edited book is intended for use by students, academics and practitioners who take interest in the outsourcing and offshoring of information technology and business services and processes. The book offers a review of the key topics in outsourcing and offshoring, populated with practical frameworks that serve as a tool kit for practitioners, academics and students. The range of topics covered in this book is wide and diverse, and represents both client and supplier perspectives on sourcing of global services. Various aspects related to the decision making process (e.g., asset transfer), learning mechanisms and organizational practices for managing outsourcing relationships are discussed in great depth. Contemporary sourcing models, including cloud services, are examined. Client dependency on the outsourcing provider, and social aspects, such as identity, are discussed in detail. Furthermore, resistance in outsourcing and failures are investigated to derive lessons as to how to avoid them and improve efficiency in outsourcing. Topics discussed in this book combine theoretical and practical insights regarding challenges that both clients and vendors face. Case studies from client and vendor organizations are used extensively throughout the book. Last but not least, the book examines current and future trends in outsourcing and offshoring, placing particular attention on the centrality of innovation in sourcing arrangements, and how innovation can be realized in outsourcing. The book is based on a vast empirical base brought together through years of extensive research by leading researchers in information systems, strategic management and operations.

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Changes in the strength of signalling between neurones are thought to provide a cellular substrate for learning and memory. In the cerebellar cortex, raising the frequency and the strength of parallel fibre (PF) stimulation leads to a long-term depression (LTD) of the strength of signalling at the synapse between PFs and Purkinje cells (PCs), which spreads to distant synapses to the same cell via a nitric oxide (NO) dependent mechanism. At the same synapse, but under conditions of reduced post-synaptic calcium activity, raised frequency stimulation (RFS) of PFs triggers a long-term potentiation of synaptic transmission. The aims of the work described in this thesis were to investigate the conditions necessary for LTD and LTP at this synapse following RFS and to identify the origins and second messenger cascades involved in the induction and spread of LTP and LTD. In thin, parasagittal cerebellar slices whole cell patch clamp recordings were made from PCs and the effects of RFS of one of two, independent PF inputs to the same PC were examined under a range of experimental conditions. Under conditions designed to reduce post-synaptic calcium activity, RFS to a single PF input led to LTP and a decreases in paired pulse facilitation (PPF) in both pathways. This heterosynaptic potentiation was prevented by inhibition of protein kinase A (PKA) or by inhibition of NO synthase with either 7-nitroindazole (7-NI) or NG Nitro-L-argenine methyl ester. Inhibition of guanylate cyclase (GC) or protein kinase G (PKG) had no effect. A similar potentiation was observed upon application of the adenylyl cyclase (AC) activator forskolin or the NO donor spermine NONOate. Both of these treatments also resulted in an increase in the frequency of mEPSCs, which provides further evidence for a presynaptic origin of LTP. Forskolin induced potentiation and the increase in mEPSC frequency were blocked by 7-NI. The styryl dye FM1-43, a fluorescent reporter of endo- and exocytosis, was also used to further examine the possible pre-synaptic origins of LTP. RFS or forskolin application enhanced FM1-43 de-staining and NOS inhibitors blocked this effect. Application of NONOate also enhanced FM1-43 de-staining. When post-synaptic calcium activity was less strictly buffered, RFS to a single PF input led to a transient potentiation that was succeeded by LTD in both pathways. This LTD, which resembled previously described forms, was prevented by inhibition of the NO/cGMP/PKG cascade. Modification of the AC/cAMP/PKA cascade had no effect. In summary, the direction of synaptic plasticity at the PF-PC synapse in response to RFS depends largely on the level of post-synaptic calcium activity. LTP and LTD were non-input specific and both forms of plasticity were dependent on NOS activity. Induction of LTP was mediated by a presynaptic mechanism and depended on NO and cAMP production. LTD on the other hand was a post-synaptic process and required activity of the NO/cGMP/PKG signalling cascade.

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The direction of synaptic plasticity at the connection between parallel fibres (PFs) and Purkinje cells can be modified by PF stimulation alone. Strong activation (Hartell, 1996) or high frequency stimulation (Schreurs and Alkon, 1993) of PFs induced a long-term depression (LTD) of PF-mediated excitatory postsynaptic currents. Brief raised frequency molecular layer stimulation produced a cAMP-dependent long-temi potentiation (LTP) of field potential (FP) responses (Salin et al., 1998). Thin slices of cerebellar vermis were prepared from 14-21 day old male Wistar rats decapitated under Halothane anaesthesia. FP's were recorded from the Purkinje cell layer in response to alternate 0.2Hz activation of stimulating electrodes placed in the molecular layer. In the presence of picrotoxin, FPs displayed two tetrodotoxin-sensitive, negative-going components termed N1 and N2. EPs were graded responses with paired pulse facilitation and were selectively blocked by 101AM 6-cyano-7-nitroquinoxaline-2,3-dicne (CNQX) an antagonist at iy,-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-type ionotropic glutamate receptors (AMPAR) suggesting that they were primarily PE-mediated. The effects of raised stimulus intensity (RS) and/or increased frequency (IF) activation of the molecular layer on FP responses were examined. In sagittai and transverse slices combined RS and IF molecular layer activation induced a LTD of the N2 component of FP responses. RSIF stimulation produced fewer incidences of LTD in sagittal slices when an inhibitor of nitric oxide synthase (NOS), guanylate cyclase (GC), protein kinase G (PKG) or the GABAB receptor antagonist CGP62349 was included into the perfusion medium. Application of a nitric oxide (NO) donor, a cyclic guanosine monophosphate (cGMP) analogue or a phosphodiesterase (PDE) type V inhibitor to prevent cGMP breakdown paired with IF stimulation produced an acute depression, Raised frequency (RF) molecular layer stimulation produced a slowly emerging LTD of N2 in sagittal slices that was largely blocked in the presence of NOS, cGMP or PKG inhibitors. In transverse slices RE stimulation produced a LTP of the N2 component that was prevented by an inhibitor of protein kinase A or NOS. Inhibition of cGMP-signalling frequently revealed an underlying potentiation suggesting that cGMP activity might mask the effects of cAMP. In sagittal slices RE stimulation resulted in a potentiation of FPs when the cAMP-specific PDE type IV inhibitor rolipram was incorporated into the perfusion medium. In summary, raised levels of PE stimulation can alter the synaptic efficacy at PF-Purkinje cell synapses. The results provide support for a role of NO/cGMP/PKG signalling in the induction of LTD in the cerebellar cortex and suggest that activation of GABAa receptors might also be important. The level of cyclic nucleotide-specific PDE activities may be crucial in determining the level of cGMP and CAMP activity and hence the direction of synaptic plasticity.

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Layer 5 contains the major projection neurons of the neocortex and is composed of two major cell types: regular spiking (RS) cells, which have cortico-cortical projections, and intrinsic bursting cells (IB), which have subcortical projections. Little is known about the plasticity processes and specifically the molecular mechanisms by which these two cell classes develop and maintain their unique integrative properties. In this study, we find that RS and IB cells show fundementally different experience-dependent plasticity processes and integrate Hebbian and homeostatic components of plasticity differently. Both RS and IB cells showed TNFα-dependent homeostatic plasticity in response to sensory deprivation, but IB cells were capable of a much faster synaptic depression and homeostatic rebound than RS cells. Only IB cells showed input-specific potentiation that depended on CaMKII autophosphorylation. Our findings demonstrate that plasticity mechanisms are not uniform within the neocortex, even within a cortical layer, but are specialized within subcircuits.

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In the Ventrobasal (VB) thalamus, astrocytes are known to elicit NMDA-receptor mediated slow inward currents (SICs) spontaneously in neurons. Fluorescence imaging of astrocytes and patch clamp recordings from the thalamocortical (TC) neurons in the VB of 6-23 day old Wistar rats were performed. TC neurons exhibit spontaneous SICs at low frequencies (~0.0015Hz) that were inhibited by NMDA-receptor antagonists D-AP5 (50µM), and were insensitive to TTX (1µM) suggesting a non-neuronal origin. The effect of corticothalamic (CT) and sensory (Sen) afferent stimulation on astrocyte signalling was assessed by varying stimulus parameters. Moderate synaptic stimulation elicited astrocytic Ca2+ increases, but did not affect the incidence of spontaneous SICs. Prolonged synaptic stimulation induced a 265% increase in SIC frequency. This increase lasted over one hour after the cessation of synaptic stimulation, so revealing a Long Term Enhancement (LTE) of astrocyte-neuron signalling. LTE induction required group I mGluR activation. LTE SICs targeted NMDA-receptors located at extrasynaptic sites. LTE showed a developmental profile: from weeks 1-3, the SIC frequency was increased by an average 50%, 240% and 750% respectively. Prolonged exposure to glutamate (200µM) increased spontaneous SIC frequency by 1800%. This “chemical” form of LTE was prevented by the broad-spectrum excitatory amino acid transporter (EAAT) inhibitor TBOA (300µM) suggesting that glutamate uptake was a critical factor. My results therefore show complex glutamatergic signalling interactions between astrocytes and neurons. Furthermore, two previously unrecognised mechanisms of enhancing SIC frequency are described. The synaptically induced LTE represents a form of non-synaptic plasticity and a glial “memory” of previous synaptic activity whilst enhancement after prolonged glutamate exposure may represent a pathological glial signalling mechanism.

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We developed a parallel strategy for learning optimally specific realizable rules by perceptrons, in an online learning scenario. Our result is a generalization of the Caticha–Kinouchi (CK) algorithm developed for learning a perceptron with a synaptic vector drawn from a uniform distribution over the N-dimensional sphere, so called the typical case. Our method outperforms the CK algorithm in almost all possible situations, failing only in a denumerable set of cases. The algorithm is optimal in the sense that it saturates Bayesian bounds when it succeeds.

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In the editorial of this special issue we argue that knowledge flows, learning and development are becoming increasingly important in all organisations operating in an international context. The possession of capabilities relating to acquisition, configuration and transfer of relevant knowledge effectively within and across different organisational units, teams, and countries is integrally related to superior organisational performance. In mastering such capabilities, internationalised organisations need to grapple with the inherent challenges relating to contextual variation and different work modes between subsidiaries, partners or team members. The papers in this special issue cast light on crucial aspects of knowledge flows, learning and development in internationalised organisations. Their contribution varies from the provision of frameworks to systematise investigation of these issues, to empirical evidence about effective mechanisms, as well as enabling and constraining forces, in facilitating knowledge transfer, learning and human capital development. © 2012 Inderscience Enterprises Ltd.

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Although the role of strategic leadership in developing organizational learning capabilities has been examined to a certain extent, the specific behaviors and mechanisms through which these capabilities are developed have not been adequately understood. Paucity of research in this direction is even more conspicuous in a small firm/entrepreneurship context, which has been linked to innovation, economic growth, and employment generation. Reporting on an ethnographic study of a knowledge-intensive, growth-oriented small firm, this article addresses this gap in the literature by integrating strategic leadership and organizational learning theory in an entrepreneurship context. In this undertaking, situated learning theory is used as the major analytical lens, to shed light on how strategic leadership can build organizational learning capabilities that underpin entrepreneurial performance in small firms. Finally, implications for situated learning theory as an organizational learning perspective and leadership practice in an entrepreneurship context are submitted. © 2012 Wiley Periodicals, Inc.

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Four bar mechanisms are basic components of many important mechanical devices. The kinematic synthesis of four bar mechanisms is a difficult design problem. A novel method that combines the genetic programming and decision tree learning methods is presented. We give a structural description for the class of mechanisms that produce desired coupler curves. Constructive induction is used to find and characterize feasible regions of the design space. Decision trees constitute the learning engine, and the new features are created by genetic programming.

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Spatial objects may not only be perceived visually but also by touch. We report recent experiments investigating to what extent prior object knowledge acquired in either the haptic or visual sensory modality transfers to a subsequent visual learning task. Results indicate that even mental object representations learnt in one sensory modality may attain a multi-modal quality. These findings seem incompatible with picture-based reasoning schemas but leave open the possibility of modality-specific reasoning mechanisms.

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Changing the whisker complement on a rodent's snout can lead to two forms of experience-dependent plasticity (EDP) in the neurons of the barrel cortex, where whiskers are somatotopically represented. One form, termed coding plasticity, concerns changes in synaptic transmission and connectivity between neurons. This is thought to underlie learning and memory processes and so adaptation to a changing environment. The second, called homeostatic plasticity, serves to maintain a restricted dynamic range of neuronal activity thus preventing its saturation or total downregulation. Current explanatory models of cortical EDP are almost exclusively neurocentric. However, in recent years, increasing evidence has emerged on the role of astrocytes in brain function, including plasticity. Indeed, astrocytes appear as necessary partners of neurons at the core of the mechanisms of coding and homeostatic plasticity recorded in neurons. In addition to neuronal plasticity, several different forms of astrocytic plasticity have recently been discovered. They extend from changes in receptor expression and dynamic changes in morphology to alteration in gliotransmitter release. It is however unclear how astrocytic plasticity contributes to the neuronal EDP. Here, we review the known and possible roles for astrocytes in the barrel cortex, including its plasticity.

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ERK1/2 is required for certain forms of synaptic plasticity, including the long-term potentiation of synaptic strength. However, the molecular mechanisms regulating synaptically localized ERK1/2 signaling are poorly understood. Here, we show that the MAPK scaffold protein kinase suppressor of Ras 1 (KSR1) is directly phosphorylated by the downstream kinase ERK1/2. Quantitative Western blot analysis further demonstrates that expression of mutated, feedback-deficient KSR1 promotes sustained ERK1/2 activation in HEK293 cells in response to EGF stimulation, compared to a more transient activation in control cells expressing wild-type KSR1. Immunocytochemistry and confocal imaging of primary hippocampal neurons from newborn C57BL6 mice further show that feedback phosphorylation of KSR1 significantly reduces its localization to dendritic spines. This effect can be reversed by tetrodotoxin (1 μM) or PD184352 (2 μM) treatment, further suggesting that neuronal activity and phosphorylation by ERK1/2 lead to KSR1 removal from the postsynaptic compartment. Consequently, electrophysiological recordings in hippocampal neurons expressing wild-type or feedback-deficient KSR1 demonstrate that KSR1 feedback phosphorylation restricts the potentiation of excitatory postsynaptic currents. Our findings, therefore, suggest that feedback phosphorylation of the scaffold protein KSR1 prevents excessive ERK1/2 signaling in the postsynaptic compartment and thus contributes to maintaining physiological levels of synaptic excitability. © FASEB.