13 resultados para firing

em Biblioteca Digital da Produção Intelectual da Universidade de São Paulo


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We study the firing rate properties of a cellular automaton model for a neuronal network with chemical synapses. We propose a simple mechanism in which the nonlocal connections are included, through electrical and chemical synapses. In the latter case, we introduce a time delay which produces self-sustained activity. Nonlocal connections, or shortcuts, are randomly introduced according to a specified connection probability. There is a range of connection probabilities for which neuron firing occurs, as well as a critical probability for which the firing ceases in the absence of time delay. The critical probability for nonlocal shortcuts depends on the network size according to a power-law. We also compute the firing rate amplification factor by varying both the connection probability and the time delay for different network sizes. (C) 2011 Elsevier B.V. All rights reserved.

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It has been revealed that the network of excitable neurons via attractive coupling can generate spikes under stimuli of subthreshold signals with disordered phases. In this paper, we explore the firing activity induced by phase disorder in excitable neuronal networks consisting of both attractive and repulsive coupling. By increasing the fraction of repulsive coupling, we find that, in the weak coupling strength case, the firing threshold of phase disorder is increased and the system response to subthreshold signals is decreased, indicating that the effect of inducing neuron firing by phase disorder is weakened with repulsive coupling. Interestingly, in the large coupling strength case, we see an opposite situation, where the coupled neurons show a rather large response to the subthreshold signals even with small phase disorder. The latter case implies that the effect of phase disorder is enhanced by repulsive coupling. A system of two-coupled excitable neurons is used to explain the role of repulsive coupling on phase-disorder-induced firing activity.

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Smoking cue-provoked craving is an intricate behavior associated with strong changes in neural networks. Craving is one of the main reasons subjects continue to smoke; therefore interventions that can modify activity in neural networks associated with craving can be useful tools in future research investigating novel treatments for smoking cessation. The goal of this study was to use a neuromodulatory technique associated with a powerful effect on spontaneous neuronal firing - transcranial direct current stimulation (tDCS) - to modify cue-provoked smoking craving. Based on preliminary data showing that craving can be modified after a single tDCS session, here we investigated the effects of repeated tDCS sessions on craving behavior. Twenty-seven subjects were randomized to receive sham or active tDCS (anodal tDCS of the left DLPFC). Our results show a significant cumulative effect of tDCS on modifying smoking cue-provoked craving. In fact, in the group of active stimulation, smoking cues had an opposite effect on craving after stimulation - it decreased craving - as compared to sham stimulation in which there was a small decrease or increase on craving. In addition, during these 5 days of stimulation there was a small but significant decrease in the number of cigarettes smoked in the active as compared to sham tDCS group. Our findings extend the results of our previous study as they confirm the notion that tDCS has a specific effect on craving behavior and that the effects of several sessions can increase the magnitude of its effect. These results open avenues for the exploration of this method as a therapeutic alternative for smoking cessation and also as a mean to change stimulus-induced behavior. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

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Based on a structured literature review, the ceramic tiles sector of Italy (benchmark) and Brazil (2nd world producer and consumer) are compared, under four strategic factors: normative, market, technology and strategic management, in order to identify critical risks for a national strategic sector. The document aims to propose guidelines for a strategic re-planning of the Brazilian ceramic tiles sector, making the Brazilian producers aware of the national market fragility (in spite of its recent remarkable evolution) and helping the policy makers to reflect on the need of reviewing the strategic planning methods and practice, of designing new targeted programs (based on coherence between operation and business strategies), of providing improved management to strengthen the sector against unfair competition by low-cost producers, enhancing the necessary infrastructure in technology, work, marketing and quality management. The analysis is limited to the single-firing production technology. The wide-coverage strategic analysis of the Brazilian ceramic tiles sector, very little studied until now in a scientific way, emphasizes the importance of applying research methodology and may be valuable to both scholars and practitioners. Additionally, it highlights the need of investments in innovation (product design and production technology) and the fundamental role of the sector organization, identifying different dimensions. It is possible to conclude that the recent Brazilian production growth is not due to a natural strengthening because of the hit of the sector and of correct enterprises strategy, but it seems the result of a temporary and favorable economic contingency.

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Chemosensitive neurons in the retrotrapezoid nucleus (RTN) regulate breathing in response to CO2/H+ changes. Their activity is also sensitive to neuromodulatory inputs from multiple respiratory centers, and thus they serve as a key nexus of respiratory control. However, molecular mechanisms that control their activity and susceptibility to neuromodulation are unknown. Here, we show in vitro and in vivo that KCNQ channels are critical determinants of RTN neural activity. In particular, we find that pharmacological block of KCNQ channels (XE991, 10 mu M) increased basal activity and CO2 responsiveness of RTN neurons in rat brain slices, whereas KCNQ channel activation (retigabine, 2-40 mu M) silenced these neurons. Interestingly, we also find that KCNQ and apamin-sensitive SK channels act synergistically to regulate firing rate of RTN chemoreceptors; simultaneous blockade of both channels led to a increase in CO2 responsiveness. Furthermore, we also show that KCNQ channels but not SK channels are downstream effectors of serotonin modulation of RTN activity in vitro. In contrast, inhibition of KCNQ channel did not prevent modulation of RTN activity by Substance P or thyrotropin-releasing hormone, previously identified neuromodulators of RTN chemoreception. Importantly, we also show that KCNQ channels are critical for RTN activity in vivo. Inhibition of KCNQ channels lowered the CO2 threshold for phrenic nerve discharge in anesthetized rats and decreased the ventilatory response to serotonin in awake and anesthetized animals. Given that serotonergic dysfunction may contribute to respiratory failure, our findings suggest KCNQ channels as a new therapeutic avenue for respiratory complications associated with multiple neurological disorders.

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Leao RM, Li S, Doiron B, Tzounopoulos T. Diverse levels of an inwardly rectifying potassium conductance generate heterogeneous neuronal behavior in a population of dorsal cochlear nucleus pyramidal neurons. J Neurophysiol 107: 3008-3019, 2012. First published February 29, 2012; doi:10.1152/jn.00660.2011.-Homeostatic mechanisms maintain homogeneous neuronal behavior among neurons that exhibit substantial variability in the expression levels of their ionic conductances. In contrast, the mechanisms, which generate heterogeneous neuronal behavior across a neuronal population, remain poorly understood. We addressed this problem in the dorsal cochlear nucleus, where principal neurons exist in two qualitatively distinct states: spontaneously active or not spontaneously active. Our studies reveal that distinct activity states are generated by the differential levels of a Ba2+-sensitive, inwardly rectifying potassium conductance (K-ir). Variability in K-ir maximal conductance causes variations in the resting membrane potential (RMP). Low K-ir conductance depolarizes RMP to voltages above the threshold for activating subthreshold-persistent sodium channels (Na-p). Once Na-p channels are activated, the RMP becomes unstable, and spontaneous firing is triggered. Our results provide a biophysical mechanism for generating neural heterogeneity, which may play a role in the encoding of sensory information.

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A growing body of evidence indiates that carbon monoxide (CO) acts as a gas neurotransmitter within the central nervous system. Although CO has been shown to affect neurohypophyseal hormone release in response to osmotic stimuli, the precise sources, targets and mechanisms underlying the actions of CO within the magnocellular neurosecretory system remain largely unknown. In the present study, we combined immunohistochemistry and patch-clamp electrophysiology to study the cellular distribution of the CO-synthase enzyme heme oxygenase type 1 (HO-1), as well as the actions of CO on oxytocin (OT) and vasopressin (VP) magnocellular neurosecretory cells (MNCs), in euhydrated (EU) and 48-h water-deprived rats (48WD). Our results show the expression of HO-1 immunoreactivity both in OT and VP neurones, as well as in a small proportion of astrocytes, both in supraoptic (SON) and paraventricular (PVN) nuclei. HO-1 expression, and its colocalisation with OT and VP neurones within the SON and PVN, was significantly enhanced in 48WD rats. Inhibition of HO activity with chromium mesoporphyrin IX chloride (CrMP; 20 mu m) resulted in a slight membrane hyperpolarisation in SON neurones from EU rats, without significantly affecting their firing activity. In 48WD rats, on the other hand, CrMP resulted in a more robust membrane hyperpolarisation, significantly decreasing neuronal firing discharge. Taken together, our results indicate that magnocellular SON and PVN neurones express HO-1, and that CO acts as an excitatory gas neurotransmitter in this system. Moreover, we found that the expression and actions of CO were enhanced in water-deprived rats, suggesting that the state-dependent up-regulation of the HO-1/CO signalling pathway contributes to enhance MNCs firing activity during an osmotic challenge.

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PURPOSE. Adequate passive-fitting of one-piece cast 3-element implant-supported frameworks is hard to achieve. This short communication aims to present an alternative method for section of one-piece cast frameworks and for casting implant-supported frameworks. MATERIALS AND METHODS. Three-unit implant-supported nickel-chromium (Ni-Cr) frameworks were tested for vertical misfit (n = 6). The frameworks were cast as one-piece (Group A) and later transversally sectioned through a diagonal axis (Group B) and compared to frameworks that were cast diagonally separated (Group C). All separated frameworks were laser welded. Only one side of the frameworks was screwed. RESULTS. The results on the tightened side were significantly lower in Group C (6.43 +/- 3.24 mu m) when compared to Groups A (16.50 +/- 7.55 mu m) and B (16.27 +/- 1.71 mu m) (P<.05). On the opposite side, the diagonal section of the one-piece castings for laser welding showed significant improvement in the levels of misfit of the frameworks (Group A, 58.66 +/- 14.30 mu m; Group B, 39.4.8 +/- 12.03 mu m; Group C, 23.13 +/- 8.24 mu m) (P<.05). CONCLUSION. Casting diagonally sectioned frameworks lowers the misfit levels. Lower misfit levels for the frameworks can be achieved by diagonally sectioning one-piece frameworks. [J Adv Prosthodont 2012;4:89-92]

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The vertebrate retina has a very high dynamic range. This is due to the concerted action of its diverse cell types. Ganglion cells, which are the output cells of the retina, have to preserve this high dynamic range to convey it to higher brain areas. Experimental evidence shows that the firing response of ganglion cells is strongly correlated with their total dendritic area and only weakly correlated with their dendritic branching complexity. On the other hand, theoretical studies with simple neuron models claim that active and large dendritic trees enhance the dynamic range of single neurons. Theoretical models also claim that electrical coupling between ganglion cells via gap junctions enhances their collective dynamic range. In this work we use morphologically reconstructed multi-compartmental ganglion cell models to perform two studies. In the first study we investigate the relationship between single ganglion cell dynamic range and number of dendritic branches/total dendritic area for both active and passive dendrites. Our results support the claim that large and active dendrites enhance the dynamic range of a single ganglion cell and show that total dendritic area has stronger correlation with dynamic range than with number of dendritic branches. In the second study we investigate the dynamic range of a square array of ganglion cells with passive or active dendritic trees coupled with each other via dendrodendritic gap junctions. Our results suggest that electrical coupling between active dendritic trees enhances the dynamic range of the ganglion cell array in comparison with both the uncoupled case and the coupled case with cells with passive dendrites. The results from our detailed computational modeling studies suggest that the key properties of the ganglion cells that endow them with a large dynamic range are large and active dendritic trees and electrical coupling via gap junctions.

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Computer simulations of external current stimulations of dentate gyrus granule cells of rats with Status Epilepticus induced by pilocarpine and control rats were used to evaluate whether morphological differences alone between these cells have an impact on their electrophysiological behavior. The cell models were constructed using morphological information from tridimensional reconstructions with Neurolucida software. To evaluate the effect of morphology differences alone, ion channel conductances, densities and distributions over the dendritic trees of dentate gyrus granule cells were the same for all models. External simulated currents were injected in randomly chosen dendrites belonging to one of three different areas of dentate gyrus granule cell molecular layer: inner molecular layer, medial molecular layer and outer molecular layer. Somatic membrane potentials were recorded to determine firing frequencies and inter-spike intervals. The results show that morphologically altered granule cells from pilocarpine-induced epileptic rats are less excitable than control cells, especially when they are stimulated in the inner molecular layer, which is the target area for mossy fibers that sprout after pilocarpine-induced cell degeneration. This suggests that morphological alterations may act as a protective mechanism to allow dentate gyrus granule cells to cope with the increase of stimulation caused by mossy fiber sprouting.

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The present study aimed determines lead (Pb), antimony (Sb) and barium (Ba) as the major elements present in GSR in the environmental air of the Ballistics Laboratory of the Sao Paulo Criminalistics Institute (I.C.-S.P.), Sao Paulo, SP, Brazil. Micro environmental monitors (mini samplers) were located at selected places. The PM2.5 fraction of this airborne was collected in, previously weighted filters, and analyzed by sector field inductively coupled plasma mass spectrometer (SF-HR-ICP-MS). The higher values of the airborne lead, antimony and barium, were found at the firing range (lead (Pb): 58.9 mu g/m(3); barium (Ba): 6.9 mu g/m(3); antimony (Sb): 7.3 mu g/m(3)). The mean value of the airborne in this room during 6 monitored days was Pb: 23.1 mu g/m(3); Ba: 2.2 mu g/m(3); Sb: 1.5 mu g/m(3). In the water tank room, the air did not show levels above the limits of concern. In general the airborne lead changed from day to day, but the barium and antimony remained constant. Despite of that, the obtained values suggest that the workers may be exposed to airborne lead concentration that can result in an unhealthy environment and could increase the risk of chronic intoxication. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

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Motor cortex stimulation is generally suggested as a therapy for patients with chronic and refractory neuropathic pain. However, the mechanisms underlying its analgesic effects are still unknown. In a previous study, we demonstrated that cortical stimulation increases the nociceptive threshold of naive conscious rats with opioid participation. In the present study, we investigated the neurocircuitry involved during the antinociception induced by transdural stimulation of motor cortex in naive rats considering that little is known about the relation between motor cortex and analgesia. The neuronal activation patterns were evaluated in the thalamic nuclei and midbrain periaqueductal gray. Neuronal inactivation in response to motor cortex stimulation was detected in thalamic sites both in terms of immunolabeling (Zif268/Fos) and in the neuronal firing rates in ventral posterolateral nuclei and centromedian-parafascicular thalamic complex. This effect was particularly visible for neurons responsive to nociceptive peripheral stimulation. Furthermore, motor cortex stimulation enhanced neuronal firing rate and Fos immunoreactivity in the ipsilateral periaqueductal gray. We have also observed a decreased Zif268, delta-aminobutyric acid (GABA), and glutamic acid decarboxylase expression within the same region, suggesting an inhibition of GABAergic interneurons of the midbrain periaqueductal gray, consequently activating neurons responsible for the descending pain inhibitory control system. Taken together, the present findings suggest that inhibition of thalamic sensory neurons and disinhibition of the neurons in periaqueductal gray are at least in part responsible for the motor cortex stimulation-induced antinociception. (C) 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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Stern JE, Sonner PM, Son SJ, Silva FC, Jackson K, Michelini LC. Exercise training normalizes an increased neuronal excitability of NTS-projecting neurons of the hypothalamic paraventricular nucleus in hypertensive rats. J Neurophysiol 107: 2912-2921, 2012. First published February 22, 2012; doi:10.1152/jn.00884.2011.-Elevated sympathetic outflow and altered autonomic reflexes, including impaired baroreflex function, are common findings observed in hypertensive disorders. Although a growing body of evidence supports a contribution of preautonomic neurons in the hypothalamic paraventricular nucleus (PVN) to altered autonomic control during hypertension, the precise underlying mechanisms remain unknown. Here, we aimed to determine whether the intrinsic excitability and repetitive firing properties of preautonomic PVN neurons that innervate the nucleus tractus solitarii (PVN-NTS neurons) were altered in spontaneously hypertensive rats (SHR). Moreover, given that exercise training is known to improve and/or correct autonomic deficits in hypertensive conditions, we evaluated whether exercise is an efficient behavioral approach to correct altered neuronal excitability in hypertensive rats. Patch-clamp recordings were obtained from retrogradely labeled PVN-NTS neurons in hypothalamic slices obtained from sedentary (S) and trained (T) Wistar-Kyoto (WKY) and SHR rats. Our results indicate an increased excitability of PVN-NTS neurons in SHR-S rats, reflected by an enhanced input-output function in response to depolarizing stimuli, a hyperpolarizing shift in Na+ spike threshold, and smaller hyperpolarizing afterpotentials. Importantly, we found exercise training in SHR rats to restore all these parameters back to those levels observed in WKY-S rats. In several cases, exercise evoked opposing effects in WKY-S rats compared with SHR-S rats, suggesting that exercise effects on PVN-NTS neurons are state dependent. Taken together, our results suggest that elevated preautonomic PVN-NTS neuronal excitability may contribute to altered autonomic control in SHR rats and that exercise training efficiently corrects these abnormalities.