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Stimulus Duration (stimulus + duration)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Cholinergic modulation of visuospatial responding in central thalamus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2007
Lori A. Newman
Abstract Central thalamus has extensive connections with basal ganglia and frontal cortex that are thought to play a critical role in sensory-guided goal-directed behavior. Central thalamic activity is influenced by cholinergic projections from mesopontine nuclei. To elucidate this function we trained rats to respond to lights in a reaction time (RT) task and compared effects of muscarinic (2.4, 7.3, 22 nmol scopolamine) and nicotinic (5.4, 16, 49, 98 nmol mecamylamine) antagonists with the GABAA agonist muscimol (0.1, 0.3, 1.0 nmol) in central thalamus. We compared this with subcutaneous (systemic) effects of mecamylamine (3.2, 9.7, 29 µmol/kg) and scopolamine (0.03, 0.09, 0.26 µmol/kg). Subcutaneous scopolamine increased omissions (failure to respond within a 3-s response window) at the highest dose tested. Subcutaneous mecamylamine increased omissions at the highest dose tested while impairing RT and per cent correct at lower doses. Intrathalamic injections of muscimol and mecamylamine decreased per cent correct at doses that did not affect omissions or RT. Intrathalamic scopolamine increased omissions and RT at doses that had little effect on per cent correct. Anatomical controls indicated that the effects of mecamylamine were localized in central thalamus and those of scopolamine were not. Drug effects did not interact with attention-demanding manipulations of stimulus duration, proximity of stimulus and response locations, or stimulus array size. These results are consistent with the hypothesis that central thalamus mediates decisional processes linking sensory stimuli with actions, downstream from systems that detect sensory signals. They also provide evidence that this function is specifically influenced by nicotinic cholinergic receptors. [source]

Ischemia,Reperfusion Impairs Ascending Vasodilation in Feed Arteries of Hamster Skeletal Muscle

MICROCIRCULATION, Issue 7 2005
MIRIAM C. J. DE WITH
ABSTRACT Objective: Vasodilation originating within the microcirculation ascends into proximal feed arteries during muscle contraction to attain peak levels of muscle blood flow. Ascending vasodilation (AVD) requires an intact endothelium, as does conducted vasodilation in response to acetylcholine (ACh). Whereas ischemia,reperfusion (I-R) can affect endothelial cell function, the effect of I-R on AVD is unknown. The authors tested the hypothesis that I-R (1h,1h) would impair AVD. Methods: Using the retractor muscle of anesthetized hamsters, contractions were evoked using field stimulation (200 ms at 40 Hz every 2 s for 1 min) and ACh was delivered using microiontophoresis (1 ,m tip, 500,4000 ms pulse at 800 nA). Feed artery responses were monitored 500,1500 ,m upstream. Results: Neither resting (51 ± 4 ,m) nor maximal diameter (81 ± 5 ,m; 10 ,m sodium nitroprusside) following I-R (n = 8) were different from time-matched controls (n = 10). With peak active tension of 23 ± 4 mN · mm,2, control AVD was 26 ± 2 ,m. Following I-R, active tension fell by 48% (p < .05) and AVD by 57% (p < .05). Stimulation at 70 Hz restored active tension but AVD remained depressed by nearly half (p < .05), as did local and conducted responses to ACh. Nevertheless, control responses to 500 ms ACh were restored by increasing stimulus duration to 4000 ms. Conclusions: Ischemia,reperfusion impairs the initiation of feed artery dilation with muscle contraction and with ACh while conduction along the vessel wall is preserved. Respective components of endothelial cell signaling events may differ in their susceptibility to I-R. [source]

After-effects of near-threshold stimulation in single human motor axons

THE JOURNAL OF PHYSIOLOGY, Issue 3 2005
Hugh Bostock
Subthreshold electrical stimuli can generate a long-lasting increase in axonal excitability, superficially resembling the phase of superexcitability that follows a conditioning nerve impulse. This phenomenon of ,subthreshold superexcitability' has been investigated in single motor axons in six healthy human subjects, by tracking the excitability changes produced by conditioning stimuli of different amplitudes and waveforms. Near-threshold 1 ms stimuli caused a mean decrease in threshold at 5 ms of 22.1 ± 6.0% (mean ±s.d.) if excitation occurred, or 6.9 ± 2.6% if excitation did not occur. The subthreshold superexcitability was maximal at an interval of about 5 ms, and fell to zero at 30 ms. It appeared to be made up of two components: a passive component linearly related to conditioning stimulus amplitude, and a non-linear active component. The active component appeared when conditioning stimuli exceeded 60% of threshold, and accounted for a maximal threshold decrease of 2.6 ± 1.3%. The passive component was directly proportional to stimulus charge, when conditioning stimulus duration was varied between 0.2 and 2 ms, and could be eliminated by using triphasic stimuli with zero net charge. This change in stimulus waveform had little effect on the active component of subthreshold superexcitability or on the ,suprathreshold superexcitability' that followed excitation. It is concluded that subthreshold superexcitability in human motor axons is mainly due to the passive electrotonic effects of the stimulating current, but this is supplemented by an active component (about 12% of suprathreshold superexcitability), due to a local response of voltage-dependent sodium channels. [source]

Differential transient MEG and fMRI responses to visual stimulation onset rate

INTERNATIONAL JOURNAL OF IMAGING SYSTEMS AND TECHNOLOGY, Issue 1 2008
August S. Tuan
Abstract While recent analysis of functional magnetic resonance imaging (fMRI) data utilize a generalized nonlinear convolution model (e.g., dynamic causal modeling), most conventional analyses of local responses utilize a linear convolution model (e.g., the general linear model). These models assume a linear relationship between the blood oxygenated level dependent (BOLD) signal and the underlying neuronal response. While previous studies have shown that this "neurovascular coupling" process is approximately linear, short stimulus durations are known to produce a larger fMRI response than expected from a linear system. This divergence from linearity between the stimulus time-course and BOLD signal could be caused by neuronal onset and offset transients, rather than a nonlinearity in the hemodynamics related to BOLD contrast. We tested this hypothesis by measuring MEG and fMRI responses to stimuli with ramped contrast onsets and offsets in place of abrupt transitions. MEG results show that the ramp successfully reduced the transient onset of neural activity. However, the nonlinearity in the fMRI response, while also reduced, remained. Predictions of fMRI responses from MEG signals show a weaker nonlinearity than observed in the actual fMRI data. These results suggest that the fMRI BOLD nonlinearity seen with short duration stimuli is not solely due to transient neuronal activity. © 2008 Wiley Periodicals, Inc. Int J Imaging Syst Technol, 18, 17,28, 2008 [source]