47 resultados para circuit neuronal moteur
em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"
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Cochlear root neurons (CRNs) are the first brainstem neurons which initiate and participate in the full expression of the acoustic startle reflex. Although it has been suggested that a cholinergic pathway from the ventral nucleus of the trapezoid body (VNTB) conveys auditory prepulses to the CRNs, the neuronal origin of the VNTB-CRNs projection and the role it may play in the cochlear root nucleus remain uncertain. To determine the VNTB neuronal type which projects to CRNs, we performed tract-tracing experiments combined with mechanical lesions, and morphometric analyses. Our results indicate that a subpopulation of non-olivocochlear neurons projects directly and bilaterally to CRNs via the trapezoid body. We also performed a gene expression analysis of muscarinic and nicotinic receptors which indicates that CRNs contain a cholinergic receptor profile sufficient to mediate the modulation of CRN responses. Consequently, we investigated the effects of auditory prepulses on the neuronal activity of CRNs using extracellular recordings in vivo. Our results show that CRN responses are strongly inhibited by auditory prepulses. Unlike other neurons of the cochlear nucleus, the CRNs exhibited inhibition that depended on parameters of the auditory prepulse such as intensity and interstimulus interval, showing their strongest inhibition at short interstimulus intervals. In sum, our study supports the idea that CRNs are involved in the auditory prepulse inhibition of the acoustic startle reflex, and confirms the existence of multiple cholinergic pathways that modulate the primary acoustic startle circuit. © 2013 Springer-Verlag Berlin Heidelberg.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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The use of the SenseWear (TM) armband (SWA), an objective monitor of physical activity, is a relatively new device used by researchers to measure energy expenditure. These monitors are practical, relatively inexpensive and easy-to-use. The aim of the present study was to assess the validity of SWAs for the measurement of energy expenditure (EE) in circuit resistance training (CRT) at three different intensities in moderately active, healthy subjects. The study subjects (17 females, 12 males) undertook CRT at 30, 50 and 70% of the 15 repetition maximum for each exercise component wearing an SWA as well as an Oxycon Mobile (OM) portable metabolic system (a gold standard method for measuring EE). The EE rose as exercise intensity increased, but was underestimated by the SWAs. For women, Bland-Altman plots showed a bias of 1.13 +/- A 1.48 METs and 32.1 +/- A 34.0 kcal in favour of the OM system, while for men values of 2.33 +/- A 1.82 METs and 75.8 +/- A 50.8 kcal were recorded.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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In this paper is presented an implementation of winner-take-all circuit using CMOS technology. In the proposed configuration the inputs are current and the outputs voltage. The simulation results show that the circuit can be a winner if its input is larger than the other by 2 mu A. The simulation also shows that the response time is 100ns at a 0.2pF load capacitance. To demonstrate the functionality of the proposed circuit, a two-input winner take all circuit was built and tested by using discrete CMOS transistor array (CD40071).
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This study analyzes an accident in which two maintenance workers suffered severe burns while replacing a circuit breaker panel in a steel mill, following model of analysis and prevention of accidents (MAPA) developed with the objective of enlarging the perimeter of interventions and contributing to deconstruction of blame attribution practices. The study was based on materials produced by a health service team in an in-depth analysis of the accident. The analysis shows that decisions related to system modernization were taken without considering their implications in maintenance scheduling and creating conflicts of priorities and of interests between production and safety; and also reveals that the lack of a systemic perspective in safety management was its principal failure. To explain the accident as merely non-fulfillment of idealized formal safety rules feeds practices of blame attribution supported by alibi norms and inhibits possible prevention. In contrast, accident analyses undertaken in worker health surveillance services show potential to reveal origins of these events incubated in the history of the system ignored in practices guided by the traditional paradigm.
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1 the actions of the alpha(1)-adrenoceptor antagonist indoramin have been examined against the contractions induced by noradrenaline in the rat vas deferens and aorta taking into account a putative neuronal uptake blocking activity of this antagonist which could. result in self-cancelling actions.2 Indoramin behaved as a simple competitive antagonist of the contractions induced by noradrenaline in the vas deferens and aorta yielding pA(2) values of 7.38 +/- 0.05 (slope = 0.98 +/- 0.03) and 6.78 +/- 0.14 (slope = 1.08 +/- 0.06), respectively.3 When the experiments were repeated in the presence of cocaine (6 mu M) the potency (pA(2)) of indoramin in antagonizing the contractions of the vas deferens to noradrenaline was increased to 8.72 +/- 0.07 (slope = 1.10 +/- 0.05) while its potency remained unchanged in the aorta (pA(2) = 6.69 +/- 0.12; slope = 1.04 +/- 0.05).4 In denervated vas deferens, indoramin antagonized the contractions to noradrenaline with a potency similar to that found in the presence of cocaine (8.79 +/- 0.07; slope = 1.09 +/- 0.06).5 It is suggested that indoramin blocks alpha(1)-adrenoceptors and neuronal uptake in rat vas deferens resulting in Schild plots with slopes not different from unity even in the absence of selective inhibition of neuronal uptake. As a major consequence of this double mechanism of action, the pA(2) values for this antagonist are underestimated when calculated in situations where the neuronal uptake is active, yielding spurious pK(B) values.
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A simple and inexpensive way to fabricate arrays of gold microelectrodes is proposed. Integrated circuit chips are sawed through their middle, normal to the longest axis, leading to destruction of the silicon circuit and rupture of the gold wires that interconnect it with the external terminals. Polishing the resulting rough surface converts the tips of the wires embedded in the chip halves into arrays of gold microdisks of about 25 mu m diameter. The number of active microelectrodes (MEs), of an array depends on the number of pins in the chip, n, being typically (n/2)-4. These MEs can be used individually or externally interconnected in any combination. X-ray images of the chips and micrographs of the resulting surface of the polished arrays have revealed variable distances between neighbor MEs, which are, however, larger than 10 times the radius of the disks. This feature of the MEs prevents diffusional cross-talk between electrodes. The use of these microdisk electrodes for analytical purposes exhibits sigmoidal voltammograms, and chronoamperometric experiments confirm the nonlinear i vs. t(1/2) plots, typical for processes where radial diffusion prevails. Satisfactory uniformity was observed for the response of each electrode of an array, indicating similarity of geometry and disk areas. The potentialities of these MEs were demonstrated by the determination of cadmium at ppb levels using square wave voltammetry with preconcentration. Due to the relative ease with which these MEs can be manufactured and their good performance in (chemical) analysis, wide applications in electrochemistry and electroanalysis is envisioned.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Pompilidotoxins (PMTXs), derived from the venom of solitary wasp has been known to facilitate synaptic transmission in the lobster neuromuscular junction, and a recent further study from rat trigeminal neurons revealed that the toxin slows Na+ channel inactivation without modifying activation process. Here we report that beta -PMTX modifies rat brain type II Na+ channel alpha -subunit (rBII) expressed in human embryonic kidney cells but fails to act on the rat heart alpha -subunit (rH1) at similar concentrations. We constructed a series of chimeric mutants of rBII and rH1 Na+ channels and compared modification of the steady-state Na+ currents by beta -PMTX. We found that a difference in a single amino acid between Glu-1616 in rBII and Gln-1615 in rH1 at the extracellular loop of D4S3-S4 is crucial for the action of beta -PMTX. PMTXs, which are small peptides with 13 amino acids, would be a potential tool for exploring a new functional moiety of Na+ channels.