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      • Common therapeutic mechanisms of pallidal deep brain stimulation for hypo- and hyperkinetic movement disorders.

        McCairn, Kevin W,Iriki, Atsushi,Isoda, Masaki American Physiological Society [etc.] 2015 journal of neurophysiology Vol.114 No.4

        <P>Abnormalities in cortico-basal ganglia (CBG) networks can cause a variety of movement disorders ranging from hypokinetic disorders, such as Parkinson's disease (PD), to hyperkinetic conditions, such as Tourette syndrome (TS). Each condition is characterized by distinct patterns of abnormal neural discharge (dysrhythmia) at both the local single-neuron level and the global network level. Despite divergent etiologies, behavioral phenotypes, and neurophysiological profiles, high-frequency deep brain stimulation (HF-DBS) in the basal ganglia has been shown to be effective for both hypo- and hyperkinetic disorders. The aim of this review is to compare and contrast the electrophysiological hallmarks of PD and TS phenotypes in nonhuman primates and discuss why the same treatment (HF-DBS targeted to the globus pallidus internus, GPi-DBS) is capable of ameliorating both symptom profiles. Recent studies have shown that therapeutic GPi-DBS entrains the spiking of neurons located in the vicinity of the stimulating electrode, resulting in strong stimulus-locked modulations in firing probability with minimal changes in the population-scale firing rate. This stimulus effect normalizes/suppresses the pathological firing patterns and dysrhythmia that underlie specific phenotypes in both the PD and TS models. We propose that the elimination of pathological states via stimulus-driven entrainment and suppression, while maintaining thalamocortical network excitability within a normal physiological range, provides a common therapeutic mechanism through which HF-DBS permits information transfer for purposive motor behavior through the CBG while ameliorating conditions with widely different symptom profiles.</P>

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        PLASMA ALLANTOIN CONCENTRATION IN RESPONSE TO CHANGES IN NUTRITIONAL STATUS OF CALVES

        Kagiyama, K.,Funaba, M.,Iriki, T.,Abe, M. Asian Australasian Association of Animal Productio 1996 Animal Bioscience Vol.9 No.2

        Two experiments were conducted to search factor(s) affecting the plasma allantoin concentration in infant calves. In experiment 1, five male Holstein calves aged 1 week were given only milk replacer free from nucleic acids for 28 days Plasma allantoin concentration varied in a reverse proportion to daily amounts of milk replacer, and the concentration when calves received 750 g/d of milk replacer was significantly lower than that when they received 250 g/d. Contrary to plasma allantoin concentration, glomerular filtration rate(GFR) was directly proportional to daily amounts of milk replacer, leading to a constant filtration of allantoin across the glomeruli. Renal handling of allantion was also unaffected by the amount of milk replacer, resulting in the constant urinary excretion of allantoin. These results suggested that GFR, which was affected by the nutritional status, could affect plasma allantoin concentration. In experiment 2, the effect of age-related changes in nutritional status after weaning on GFR was examined in eight calves weaned at 5 weeks of age. The GFR expressed as body weight basis was lower immediately after weaning, but linearly increased up to the 19th week post-weaning. The present results suggested that the changes in GFR in response to nutritional status would be one of the possible causes of atypical plasma allantoin concentration immediately after weaning. We conclude that plasma allantoin concentration would not be a proper estimator of intestinal flow of microbial protein in cattle.

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        A Primary Role for Nucleus Accumbens and Related Limbic Network in Vocal Tics

        McCairn, Kevin W.,Nagai, Y.,Hori, Y.,Ninomiya, T.,Kikuchi, E.,Lee, J.Y.,Suhara, T.,Iriki, A.,Minamimoto, T.,Takada, M.,Isoda, M.,Matsumoto, M. Cell Press 2016 Neuron Vol.89 No.2

        <P>Inappropriate vocal expressions, e.g., vocal tics in Tourette syndrome, severely impact quality of life. Neural mechanisms underlying vocal tics remain unexplored because no established animal model representing the condition exists. We report that unilateral disinhibition of the nucleus accumbens (NAc) generates vocal tics in monkeys. Whole-brain PET imaging identified prominent, bilateral limbic cortico-subcortical activation. Local field potentials (LFPs) developed abnormal spikes in the NAc and the anterior cingulate cortex (ACC). Vocalization could occur without obvious LFP spikes, however, when phase-phase coupling of alpha oscillations were accentuated between the NAc, ACC, and the primary motor cortex. These findings contrasted with myoclonic motor tics induced by disinhibition of the dorsolateral putamen, where PET activity was confined to the ipsilateral sensorimotor system and LFP spikes always preceded motor tics. We propose that vocal tics emerge as a consequence of dysrhythmic alpha coupling between critical nodes in the limbic and motor networks.</P>

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