951 resultados para Slow potentials


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Mode of access: Internet.

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Running title: Electrode potentials.

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Mode of access: Internet.

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"First printing November, 1938."

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"Research supported by the McDonnell Aircraft Corporation under Contract no. 6140-20 P.O. 7S4899-R and by the Purdue Research Foundation."

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Background. The rate of binocular rivalry has been reported to be slower in subjects with bipolar disorder than in controls when tested with drifting, vertical and horizontal gratings of high spatial frequency. Method. Here we assess the rate of binocular rivalry with stationary, vertical and horizontal gratings of low spatial frequency in 30 subjects with bipolar disorder, 30 age- and sex-matched controls, 18 subjects with schizophrenia and 18 subjects with major depression. Along with rivalry rate, the predominance of each of the rivaling images was assessed, as was the distribution of normalized rivalry intervals. Results. The bipolar group demonstrated significantly slower rivalry than the control, schizophrenia and major depression groups. The schizophrenia and major depression groups did not differ significantly from the control group. Predominance values did not differ according to diagnosis and the distribution of normalized rivalry intervals was well described by a gamma function in all groups. Conclusions. The results provide further evidence that binocular rivalry is slow in bipolar disorder and demonstrate that rivalry predominance and the distribution of normalized rivalry intervals are not abnormal in bipolar disorder. It is also shown by comparison with previous work, that high strength stimuli more effectively distinguish bipolar from control subjects than low strength stimuli. The data on schizophrenia and major depression suggest the need for large-scale specificity trials. Further study is also required to assess genetic and pathophysiological factors as well as the potential effects of state, medication, and clinical and biological subtypes.

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Previous studies have reported that patients with schizophrenia demonstrate impaired performance during working memory (WM) tasks. The current study aimed to determine whether WM impairments in schizophrenia are accompanied by reduced slow wave (SW) activity during on-line maintenance of mnemonic information. Event-related potentials were obtained from patients with schizophrenia and well controls as they performed a visuospatial delayed response task. On 50% of trials, a distractor stimulus was introduced during the delay. Compared with controls, patients with schizophrenia produced less SW memory negativity, particularly over the right hemisphere, together with reduced frontal enhancement of SW memory negativity in response to distraction. The results indicate that patients with schizophrenia generate less maintenance phase neuronal activity during WM performance, especially under conditions of distraction.

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The efficiency of inhibitory control processes has been proposed as a mechanism constraining working-memory capacity. In order to investigate genetic influences on processes that may reflect interference control, event-related potential (ER-P) activity recorded at frontal sites, during distracting and nondistracting conditions of a working-memory task, in a sample of 509 twin pairs was examined. The ERP component of interest was the slow wave (SW). Considerable overlap in source of genetic influence was found, with a common genetic factor accounting for 37 - 45% of SW variance irrespective of condition. However, 3 - 8 % of SW variance in the distracting condition was influenced by an independent genetic source. These results suggest that neural responses to irrelevant and distracting information, that may disrupt working-memory performance, differ in a fundamental way from perceptual and memory-based processing in a working-memory task. Furthermore, the results are consistent with the view that cognition is a complex genetic trait influenced by numerous genes of small influence.

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We present a new approach accounting for the nonadditivity of attractive parts of solid-fluid and fluidfluid potentials to improve the quality of the description of nitrogen and argon adsorption isotherms on graphitized carbon black in the framework of non-local density functional theory. We show that the strong solid-fluid interaction in the first monolayer decreases the fluid-fluid interaction, which prevents the twodimensional phase transition to occur. This results in smoother isotherm, which agrees much better with experimental data. In the region of multi-layer coverage the conventional non-local density functional theory and grand canonical Monte Carlo simulations are known to over-predict the amount adsorbed against experimental isotherms. Accounting for the non-additivity factor decreases the solid-fluid interaction with the increase of intermolecular interactions in the dense adsorbed fluid, preventing the over-prediction of loading in the region of multi-layer adsorption. Such an improvement of the non-local density functional theory allows us to describe experimental nitrogen and argon isotherms on carbon black quite accurately with mean error of 2.5 to 5.8% instead of 17 to 26% in the conventional technique. With this approach, the local isotherms of model pores can be derived, and consequently a more reliab * le pore size distribution can be obtained. We illustrate this by applying our theory against nitrogen and argon isotherms on a number of activated carbons. The fitting between our model and the data is much better than the conventional NLDFT, suggesting the more reliable PSD obtained with our approach.

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Pyramidal neurons in the lateral amygdala discharge trains of action potentials that show marked spike frequency adaptation, which is primarily mediated by activation of a slow calcium-activated potassium current. We show here that these neurons also express an alpha-dendrotoxin- and tityustoxin-Kalpha-sensitive voltage-dependent potassium current that plays a key role in the control of spike discharge frequency. This current is selectively targeted to the primary apical dendrite of these neurons. Activation of mu-opioid receptors by application of morphine or D-Ala(2)-N-Me-Phe(4)-Glycol(5)-enkephalin (DAMGO) potentiates spike frequency adaptation by enhancing the alpha-dendrotoxin-sensitive potassium current. The effects of mu-opioid agonists on spike frequency adaptation were blocked by inhibiting G-proteins with N-ethylmaleimide (NEM) and by blocking phospholipase A(2). Application of arachidonic acid mimicked the actions of DAMGO or morphine. These results show that mu-opioid receptor activation enhances spike frequency adaptation in lateral amygdala neurons by modulating a voltage-dependent potassium channel containing Kv1.2 subunits, through activation of the phospholipase A(2)-arachidonic acid-lipoxygenases cascade.

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We sought to determine if the velocity of an acute bout of eccentric contractions influenced the duration and severity of several common indirect markers of muscle damage. Subjects performed 36 maximal fast (FST, n=8: 3.14 rad center dot s(-1)) or slow (SLW, n=7: 0.52 rad center dot s(-1)) velocity isokinetic eccentric contractions with the elbow flexors of the non-dominant arm. Muscle soreness, limb girth, plasma creatine kinase (CK) activity, isometric torque and concentric and eccentric torque at 0.52 and 3.14 rad center dot s(-1) were assessed prior to and for several days following the eccentric bout. Peak plasma CK activity was similar in SLW (4030 +/- 1029 U center dot l(-1)) and FST (5864 +/- 2664 U center dot l(-1)) groups, (p > 0.05). Both groups experienced similar decrement in all strength variables during the 48 hr following the eccentric bout. However, recovery occurred more rapidly in the FST group during eccentric (0.52 and 3.14 rad center dot s(-1)) and concentric (3.14 rad center dot s(-1)) post-testing. The severity of muscle soreness was similar in both groups. However, the FST group experienced peak muscle soreness 48 hr later than the SLW group (24 hr vs. 72 hr). The SLW group experienced a greater increase in upper arm girth than the FST group 20 min, 24 hr and 96 hr following the eccentric exercise bout. The contraction velocity of an acute bout of eccentric exercise differentially influences the magnitude and time course of several indirect markers of muscle damage.

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The calcium-dependent afterhyperpolarization (AHP) that follows trains of action potentials is responsible for controlling action potential firing patterns in many neuronal cell types. We have previously shown that the slow AHP contributes to spike frequency adaptation in pyramidal neurons in the rat lateral amygdala. In addition, a dendritic voltage-gated potassium current mediated by Kv1.2-containing channels also suppresses action potential firing in these neurons. In this paper we show that this voltage-gated potassium current and the slow AHP act together to control spike frequency adaptation in lateral amygdala pyramidal neurons. The two currents have similar effects on action potential number when firing is evoked either by depolarizing current injections or by synaptic stimulation. However, they differ in their control of firing frequency, with the voltage-gated potassium current but not the slow AHP determining the initial frequency of action potential firing. This dual mechanism of controlling firing patterns is unique to lateral amygdala neurons and is likely to contribute to the very low levels of firing seen in lateral amygdala neurons in vivo.