The use of artificial neural networks in the motor program

Though it is commonly assumed that the brain creates 'motor programs' which store the information essential to perform a motor skill, little direct evidence exists for such motor programs. Electromyography (EMG) provides a look into the motoneurons - level of a movement by measuring the electrical activity in relation to the muscle's involvement in the movement In this paper, artificial neural networks (ANNs) were applied to define the temporal patterns of EMG activity used by normal subjects in performing step-tracking tasks, and how such patterns change with practice. Our results demonstrate that ANNs could be trained to detect the input-output relationship between muscles' onset times and reaction times, and provided evidence to support the existence of a motor program.published_or_final_versio

Food properties that influence neuromuscular activity during human mastication

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Motor programs: an artificial neural network approach

It is commonly assumed that, during learning, the brain creates “motor programs” which store all the information essential to performing a motor skill. Yet there is still no consensus on what constitutes a motor program. In this study, a Multilayer Perceptron (MLP) network with one hidden layer, trained using the backpropagation rule, was used in an attempt to identify motor programs. Nine healthy subjects were asked to use their left hand to make fast and accurate movements in a tracking task of 75 identical steps, by either wrist flexion and extension, or the precision grip. The electromyogram (EMG) activity of 8 finger and hand muscles were simultaneously recorded by standard techniques. Onset timing of muscle activities were quantified from the digitized EMG signals, and were then used as the inputs to the MLP network. Reaction time was also measured, providing the desired output of the network. The trained network captured salient features of the relationship between EMG onset times and reaction time.published_or_final_versio

The Mitochondrial Calcium Uniporter participates in Ischemia/Reperfusion Injury and in Cardioprotection by Ischemic Preconditioning

The objective of the present study was to determine whether the mitochondrial calcium uniporter plays a role in cardioprotection by ischemic preconditioning (IPC). Isolated rat hearts were subjected to 30 min regional ischemia by ligation of the left anterior descending artery followed by 120 min reperfusion. We found that both IPC and inhibition of the mitochondrial calcium uniporter during reperfusion improved recovery of left ventricular developed pressure, maximal rise velocity and end-diastolic pressure, and reduced infarct size and lactate dehydrogenase release. These protective effects were attenuated by activating the mitochondrial calcium uniporter. We conclude that the mitochondrial calcium uniporter is involved in the cardioprotection of ischemic preconditioning.published_or_final_versio

Dorsal column is not involved in the mechanism of the hypotensive effect by simulating acupuncture on rat hindlimb

The present study investigated the role of the dorsal column (DC) in the mechanism of the hypotensive effect induced by simulating acupuncture on rat hindlimb. The femoral arterial pressure and electrocardiogram (ECG) of rats were recorded when the hypothalamic paraventricular nucleus (PVN) was electrically stimulated with or without DC lesion. Stimulation of the deep peroneal nerve (DPN) decreased the pressor response elicited by electrical stimulation of the PVN. Thirty minutes after micro-dissection of the right DC, the inhibitory effect of stimulating the right or left DPN on the pressor response induced by stimulation of the contralateral PVN was not altered. Of 6 rats tested, the inhibitory effect of stimulating the right or left DPN could still be observed five days after the right DC was destroyed. The pain responses of both hindlimbs of the rats with the right DC destroyed showed no obvious difference when compared with the sham control rats. These data suggest that the DC is not involved in the inhibitory effect of stimulating the DPN on the pressor response induced by the PVN activation.published_or_final_versio

Alterations of coronary perfusion pressure and cardiac contraction during lipopolysaccharide challenge

In the present study, we used the Langendorff technique to evaluate the involvement of endothelin-1 (ET-I) and nitric oxide (NO) in coronary vasoconstriction and myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats. Coronary perfusion pressure (CPP) increased markedly in hearts from LPS -treated rats. Pretreatment with BQ-123, an ET-1 type A receptor antagonist, significantly reduced the increase in CPP induced by LPS. LPS induced a marked decrease in left ventricular developed pressure, the product of left ventricular developed pressure and heart rate, as well as the maximal rate of rise/fall of left ventricular pressure. Pretreatment with BQ-123 partially reversed the LPS-induced cardiac depression. Administration of BQ-123 and AMG, an inhibitor of iNOS, prior to LPS challenge significantly blocked the negative inotropic effect. These results suggest that ET-1 augments the NO-mediated cardiac contractile depression induced by LPS and the accompanying increase in coronary resistance.published_or_final_versio

Role of the Mitochondrial Permeability Transition Pore in TNF-α -Induced Recovery of Ventricular Contraction and Reduction of Infarct Size in Isolated Rat Hearts Subjected to Ischemia/Reperfusion

Pretreatment with tumor necrosis factor-α (TNF-α) is known to trigger cardioprotection. TNF-α can activate multiple downstream signaling cascades. However, it is not known whether the mitochondrial permeability transition pore (MitoPTP) is involved in TNF-α -induced cardioprotection. In the present study, we examined whether TNF-α inhibits MitoPTP opening. In isolated rat hearts subjected to 30 min regional ischemia and 120 min reperfusion, pretreatment with 10 U/ml TNF-α for 7 min followed by 10 min washout improved the recovery of left ventricular developed pressure (LVDP) and rate-pressure product (RPP = LVDP × heart rate) during reperfusion and reduced the infarct size. Administration of 20 μ mol/L atractyloside, a MitoPTP opener, for 20 min (last 5 min of ischemia and first 15 min of reperfusion) and pretreatment with 1 μ inhibitor of the Ca2+-activated K+mol/L paxilline, an channel, for 5 min before ischemia, attenuated the recovery of LVDP and RPP and the reduction of infarct size induced by TNF-α. The findings indicate that, in the isolated heart model, TNF-α protects myocardium against ischemia/reperfusion injury via inhibiting MitoPTP opening as well as by activating the Ca2+-activated K+channel.published_or_final_versio

Vasorelaxant effect of total flavones from Dendranthema morifolium on rat thoracic aorta

To investigate the vasorelaxant effect of total flavones from Dendranthema morifolium (Ramat.) Tzvel. cv. Hangju (FDM), tension was recorded from rat thoracic aortic rings. FDM completely relaxed, in a dose-dependent manner, the contractions induced by either phenylephrine (PE) or a high concentration of KCl (60 mM) in rings with intact endothelium. Mechanical removal of the endothelium did not significantly modify the vasorelaxant effect of FDM. In endothelium-denuded aortic rings depolarized by 60 mM KCl, FDM inhibited Ca/sup 2+/-induced contraction. FDM also reduced the transient contraction elicited by PE in Ca/sup 2+/-free medium, but had no effect on active phorbol ester-induced contraction. Pretreatment of endothelium-denuded aorta with propranolol, a beta-adrenoceptor antagonist, significantly attenuated the relaxant effect of FDM. These results indicate that FDM induces an endothelium-independent relaxation in rat aortic rings. The mechanisms may include the activation of beta-adrenergic receptors, reduction in Ca/sup 2+/ influx through the voltage-dependent and receptor-operated channels, and inhibition of intracellular Ca release in vascular smooth muscle cells.published_or_final_versio

Influence of interleukin-2 on Ca2+ handling in rat ventricular myocytes

In the present study, we examined the effect of interleukin-2 (IL-2) on cardiomyocyte Ca2+ handling. The effects of steady-state and transient changes in stimulation frequency on the intracellular Ca2+ transient were investigated in isolated ventricular myocytes by spectrofluorometry. In the steady state (0.2 Hz) IL-2 (200 U/ml) decreased the amplitude of Ca2+ transients induced by electrical stimulation and caffeine. At 1.25 mM extracellular Ca2+ concentration ([Ca 2+]o), when the stimulation frequency increased from 0.2 to 1.0 Hz, diastolic Ca2+ level and peak intracellular Ca 2+ concentration ([Ca2+]i), as well as the amplitude of the transient, increased. The positive frequency relationships of the peak and amplitude of [Ca2+]i transients were blunted in the IL-2-treated myocytes. The effect of IL-2 on the electrically induced [Ca2+]i transient was not normalized by increasing [Ca2+]o to 2.5 mM. IL-2 inhibited the frequency relationship of caffeine-induced Ca2+ release. Blockade of sarcoplasmic reticulum (SR) Ca2+-ATPase with thapsigargin resulted in a significant reduction of the amplitude-frequency relationship of the transient similar to that induced by IL-2. The restitutions were not different between control and IL-2 groups at 1.25 mM [Ca2+]o, which was slowed in IL-2-treated myocytes when [Ca2+]o was increased to 2.5 mM. There was no difference in the recirculation fraction (RF) between control and IL-2-treated myocytes at both 1.25 and 2.5 mM [Ca 2+]o. The effects of IL-2 on frequency relationship, restitution, and RF may be due to depressed SR functions and an increased Na+-Ca2+ exchange activity, but not to any change in L-type Ca2+ channels. © 2003 Elsevier Ltd. All rights reserved.postprin

Simple, Fast and Accurate Implementation of the Diffusion Approximation Algorithm for Stochastic Ion Channels with Multiple States

The phenomena that emerge from the interaction of the stochastic opening and closing of ion channels (channel noise) with the non-linear neural dynamics are essential to our understanding of the operation of the nervous system. The effects that channel noise can have on neural dynamics are generally studied using numerical simulations of stochastic models. Algorithms based on discrete Markov Chains (MC) seem to be the most reliable and trustworthy, but even optimized algorithms come with a non-negligible computational cost. Diffusion Approximation (DA) methods use Stochastic Differential Equations (SDE) to approximate the behavior of a number of MCs, considerably speeding up simulation times. However, model comparisons have suggested that DA methods did not lead to the same results as in MC modeling in terms of channel noise statistics and effects on excitability. Recently, it was shown that the difference arose because MCs were modeled with coupled activation subunits, while the DA was modeled using uncoupled activation subunits. Implementations of DA with coupled subunits, in the context of a specific kinetic scheme, yielded similar results to MC. However, it remained unclear how to generalize these implementations to different kinetic schemes, or whether they were faster than MC algorithms. Additionally, a steady state approximation was used for the stochastic terms, which, as we show here, can introduce significant inaccuracies. We derived the SDE explicitly for any given ion channel kinetic scheme. The resulting generic equations were surprisingly simple and interpretable - allowing an easy and efficient DA implementation. The algorithm was tested in a voltage clamp simulation and in two different current clamp simulations, yielding the same results as MC modeling. Also, the simulation efficiency of this DA method demonstrated considerable superiority over MC methods.Comment: 32 text pages, 10 figures, 1 supplementary text + figur