52 research outputs found

    Measuring Knowledge Spillovers Using Belgian EPO and USPTO Patent Data

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    This paper investigates two major issues of the patenting behavior of Belgian firms. Firstly, it studies the probabilistic distribution of the patent citations among several major sectors. Secondly, the firm-oriented data is studied to investigate the relationships between the Belgian firms’ size and their patent citation behavior. The modeling results conclude that there is evidence that the smaller firms tend to be more active in patent citation than larger ones. Analyzing the implications from the probabilistic models of citations the paper concludes, that there are different patterns of citation behavior in different sectors. Some sectors exhibit more openness toward inter-firm or inter-industry spillovers, while others do not. Moreover, different industrial sectors exhibit different relationships between the probability of a citation to occur in this sector and the relative time lag between the citing and cited patents.

    Slow GABAA mediated synaptic transmission in rat visual cortex

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    <p>Abstract</p> <p>Background</p> <p>Previous reports of inhibition in the neocortex suggest that inhibition is mediated predominantly through GABA<sub>A </sub>receptors exhibiting fast kinetics. Within the hippocampus, it has been shown that GABA<sub>A </sub>responses can take the form of either fast or slow response kinetics. Our findings indicate, for the first time, that the neocortex displays synaptic responses with slow GABA<sub>A </sub>receptor mediated inhibitory postsynaptic currents (IPSCs). These IPSCs are kinetically and pharmacologically similar to responses found in the hippocampus, although the anatomical specificity of evoked responses is unique from hippocampus. Spontaneous slow GABA<sub>A </sub>IPSCs were recorded from both pyramidal and inhibitory neurons in rat visual cortex.</p> <p>Results</p> <p>GABA<sub>A </sub>slow IPSCs were significantly different from fast responses with respect to rise times and decay time constants, but not amplitudes. Spontaneously occurring GABA<sub>A </sub>slow IPSCs were nearly 100 times less frequent than fast sIPSCs and both were completely abolished by the chloride channel blocker, picrotoxin. The GABA<sub>A </sub>subunit-specific antagonist, furosemide, depressed spontaneous and evoked GABA<sub>A </sub>fast IPSCs, but not slow GABA<sub>A</sub>-mediated IPSCs. Anatomical specificity was evident using minimal stimulation: IPSCs with slow kinetics were evoked predominantly through stimulation of layer 1/2 apical dendritic zones of layer 4 pyramidal neurons and across their basal dendrites, while GABA<sub>A </sub>fast IPSCs were evoked through stimulation throughout the dendritic arborization. Many evoked IPSCs were also composed of a combination of fast and slow IPSC components.</p> <p>Conclusion</p> <p>GABA<sub>A </sub>slow IPSCs displayed durations that were approximately 4 fold longer than typical GABA<sub>A </sub>fast IPSCs, but shorter than GABA<sub>B</sub>-mediated inhibition. The anatomical and pharmacological specificity of evoked slow IPSCs suggests a unique origin of synaptic input. Incorporating GABA<sub>A </sub>slow IPSCs into computational models of cortical function will help improve our understanding of cortical information processing.</p

    At clinically relevant concentrations the anaesthetic/amnesic thiopental but not the anticonvulsant phenobarbital interferes with hippocampal sharp wave-ripple complexes

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    <p>Abstract</p> <p>Background</p> <p>Many sedative agents, including anesthetics, produce explicit memory impairment by largely unknown mechanisms. Sharp-wave ripple (SPW-R) complexes are network activity thought to represent the neuronal substrate for information transfer from the hippocampal to neocortical circuits, contributing to the explicit memory consolidation. In this study we examined and compared the actions of two barbiturates with distinct amnesic actions, the general anesthetic thiopental and the anticonvulsant phenobarbital, on in vitro SPW-R activity.</p> <p>Results</p> <p>Using an in vitro model of SPW-R activity we found that thiopental (50–200 μM) significantly and concentration-dependently reduced the incidence of SPW-R events (it increased the inter-event period by 70–430 %). At the concentration of 25 μM, which clinically produces mild sedation and explicit memory impairment, thiopental significantly reduced the quantity of ripple oscillation (it reduced the number of ripples and the duration of ripple episodes by 20 ± 5%, n = 12, <it>P </it>< 0.01), and suppressed the rhythmicity of SPWs by 43 ± 15% (n = 6, <it>P </it>< 0.05). The drug disrupted the synchrony of SPWs within the CA1 region at 50 μM (by 19 ± 12%; n = 5, <it>P </it>< 0.05). Similar effects of thiopental were observed at higher concentrations. Thiopental did not affect the frequency of ripple oscillation at any of the concentrations tested (10–200 μM). Furthermore, the drug significantly prolonged single SPWs at concentrations ≥50 μM (it increased the half-width and the duration of SPWs by 35–90 %). Thiopental did not affect evoked excitatory synaptic potentials and its results on SPW-R complexes were also observed under blockade of NMDA receptors. Phenobarbital significantly accelerated SPWs at 50 and 100 μM whereas it reduced their rate at 200 and 400 μM. Furthermore, it significantly prolonged SPWs, reduced their synchrony and reduced the quantity of ripples only at the clinically very high concentration of 400 μM, reported to affect memory.</p> <p>Conclusion</p> <p>We hypothesize that thiopental, by interfering with SPW-R activity, through enhancement of the GABA<sub>A </sub>receptor-mediated transmission, affects memory processes which involve hippocampal circuit activation. The quantity but not the frequency of ripple oscillation was affected by the drug.</p

    Phase-amplitude coupled persistent theta and gamma oscillations in rat primary motor cortex in vitro

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    In vivo, theta (4-7 Hz) and gamma (30-80 Hz) neuronal network oscillations are known to coexist and display phase-amplitude coupling (PAC). However, in vitro, these oscillations have for many years been studied in isolation. Using an improved brain slice preparation technique we have, using co-application of carbachol (10 μM) and kainic acid (150 nM), elicited simultaneous theta (6.6 ± 0.1 Hz) and gamma (36.6 ± 0.4 Hz) oscillations in rodent primary motor cortex (M1). Each oscillation showed greatest power in layer V. Using a variety of time series analyses we detected significant cross-frequency coupling 74% of slice preparations. Differences were observed in the pharmacological profile of each oscillation. Thus, gamma oscillations were reduced by the GABAA receptor antagonists, gabazine (250 nM and 2 μM), and picrotoxin (50 μM) and augmented by AMPA receptor antagonism with SYM2206 (20 μM). In contrast, theta oscillatory power was increased by gabazine, picrotoxin and SYM2206. GABAB receptor blockade with CGP55845 (5 μM) increased both theta and gamma power, and similar effects were seen with diazepam, zolpidem, MK801 and a series of metabotropic glutamate receptor antagonists. Oscillatory activity at both frequencies was reduced by the gap junction blocker carbenoxolone (200 μM) and by atropine (5 μM). These data show theta and gamma oscillations in layer V of rat M1 in vitro are cross-frequency coupled, and are mechanistically distinct. The development of an in vitro model of phase-amplitude coupled oscillations will facilitate further mechanistic investigation of the generation and modulation of coupled activity in mammalian cortex

    R&amp;D and Production Behavior of Asymmetric Duopoly Subject to Knowledge Spillovers

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    We construct an asymmetric duopolistic R&amp;D and production behavior model subject to knowledge spillovers. This model is an extension to the symmetric model of d&apos;Aspremont and Jacquemin (A&amp;J (1988)) and aims to determine the cooperative and non-cooperative R&amp;D strategies for two agents of different size. The paper concludes that the introduction of asymmetry into the A&amp;J (1988) model leads to different R&amp;D expenditures and production decisions made by the firms. Simulations show that the bigger agent has larger R&amp;D expenditures and higher output. If firms choose the monopoly collusion or the welfaremaximizing strategy, the optimal solution implies that R&amp;D is conducted asymmetrically by both agents, but that production is conducted only by the largest agent

    Knowledge spillovers in Belgium: Evidence from the firm's patent citation behaviour

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    This paper conducts a comprehensive study of both intra-office and cross-office patent citations indicated in patents granted to Belgian corporate applicants by the United States and European patent offices during the period between 1996 and 2000. It employs a qualitative response variable analysis (with possibly asymmetric probability distribution) to patent citations in different industries. The modeling results conclude that there are different patterns of citation behavior in patents, which belong to different industrial classes. Patents in some industries are more likely to have inter-firm or inter-industry spillovers, but there are industries with more intra-firm or intra-industry patent citation patterns. Concerning the relationship between the probability of a citation to occur in a particular industry and the relative time lag between the citing and cited patents, we also observe different pictures depending on the industry of the citing patent. In general, successful R&D cooperation stimulating policies must take into account those differences in order to balance market driven incentives and direct interventions.
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