Now showing 1 - 9 of 9
  • 2003Journal Article Discussion
    [["dc.bibliographiccitation.firstpage","2220"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Clinical Neurophysiology"],["dc.bibliographiccitation.lastpage","2222"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Nitsche, M. A."],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Lang, N."],["dc.contributor.author","Antal, Andrea"],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T10:34:56Z"],["dc.date.available","2018-11-07T10:34:56Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1016/S1388-2457(03)00235-9"],["dc.identifier.isi","000186563700026"],["dc.identifier.pmid","14580622"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44984"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","1388-2457"],["dc.title","Safety criteria for transcranial direct current stimulation (tDCS) in humans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]
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  • 2008Journal Article
    [["dc.bibliographiccitation.firstpage","2122"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neuropsychologia"],["dc.bibliographiccitation.lastpage","2128"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Kuo, Min-Fang"],["dc.contributor.author","Unger, Mandy"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Lang, Nicolas"],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Nitsche, Michael A."],["dc.date.accessioned","2018-11-07T11:20:28Z"],["dc.date.available","2018-11-07T11:20:28Z"],["dc.date.issued","2008"],["dc.description.abstract","Neuroplasticity is the adaptive modification of network connectivity in response to environmental demands and has been identified as a major physiological correlate of learning. Since unrestricted neuroplastic modifications of network connectivity will result in a cle-stabilization of the system, metaplastic modification rules have been proposed for keeping plastic connectivity changes within a useful dynamic range. In this connection, the modification threshold to achieve synaptic strengthening is thought to correlate negatively with the history of activity of the respective neurons, i.e. high previous activity enhances the threshold for synaptic strengthening and vice versa. However, the relevance of metaplasticity for actual learning processes has not been tested so far. We reduced or enhanced motor cortex excitability before performance of the serial reaction time task (SRTT), a sequential motor learning paradigm, and a reaction time task (RTT) by transcranial direct current stimulation (tDCS). If homeostatic rules apply, excitability-diminishing cathodal tDCS should improve subsequent motor learning, especially if combined with the partial NMDA receptor-agoniSt D-cycloserine, which selectively enhances efficacy of active receptors, while excitability-enhancing anodal tDCS should reduce it. Only the results for anodal tDCS, when combined with D-cycloserine, were in accordance with the rules of homeostatic plasticity. We conclude that homeostatic plasticity, as tested here, has a limited influence on implicit sequential motor learning. (C) 2008 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuropsychologia.2008.02.023"],["dc.identifier.isi","000257530800002"],["dc.identifier.pmid","18394661"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0028-3932"],["dc.title","Limited impact of homeostatic plasticity on motor learning in humans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2005Journal Article
    [["dc.bibliographiccitation.firstpage","323"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Brain Research"],["dc.bibliographiccitation.lastpage","333"],["dc.bibliographiccitation.volume","164"],["dc.contributor.author","Tings, T."],["dc.contributor.author","Lang, N."],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Sommer, M."],["dc.date.accessioned","2018-11-07T09:07:06Z"],["dc.date.available","2018-11-07T09:07:06Z"],["dc.date.issued","2005"],["dc.description.abstract","Specific stimulation of neuronal circuits may promote selective inhibition or facilitation of corticospinal tract excitability. Monophasic stimulation is more likely to achieve direction-specific neuronal excitation. In 10 healthy subjects, we compared four types of repetitive transcranial magnetic stimulation (rTMS), monophasic and biphasic stimuli with the initial current in the brain flowing antero-posteriorly (\"posteriorly directed\") or postero-anteriorly (\"anteriorly directed\"). We applied rTMS over the primary motor cortex contralateral to the dominant hand, using 80 stimuli at 5 Hz frequency at an intensity yielding baseline motor evoked potential (MEP) amplitudes of 1 mV. Monophasic stimulation was always more efficient than biphasic. Facilitation was induced by intracerebral anteriorly directed current flow and inhibition by posteriorly oriented current flow, although only initially for approximately 30 pulses. The early inhibition was absent when studied during a tonic muscle contraction. Several mechanisms could account for these findings. They include a more efficient excitation of inhibiting circuits by posteriorly oriented pulses, and a back-propagating D-wave inhibiting early I-waves and thus inducing early inhibition of MEP amplitude. In any case biphasic rTMS results can be explained by a mixture of monophasic opposite stimulations. We propose the use of monophasic pulses for maximizing effects during rTMS."],["dc.identifier.doi","10.1007/s00221-005-2253-6"],["dc.identifier.isi","000230625100005"],["dc.identifier.pmid","15868175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25712"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0014-4819"],["dc.title","Orientation-specific fast rTMS maximizes corticospinal inhibition and facilitation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2003Journal Article
    [["dc.bibliographiccitation.firstpage","293"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","301"],["dc.bibliographiccitation.volume","553"],["dc.contributor.author","Nitsche, M. A."],["dc.contributor.author","Fricke, K. J."],["dc.contributor.author","Henschke, U."],["dc.contributor.author","Schlitterlau, A."],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Lang, N."],["dc.contributor.author","Henning, S."],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T10:34:43Z"],["dc.date.available","2018-11-07T10:34:43Z"],["dc.date.issued","2003"],["dc.description.abstract","Transcranial direct current stimulation (tDCS) of the human motor cortex results in polarity-specific shifts of cortical excitability during and after stimulation. Anodal tDCS enhances and cathodal stimulation reduces excitability. Animal experiments have demonstrated that the effect of anodal tDCS is caused by neuronal depolarisation, while cathodal tDCS hyperpolarises cortical neurones. However, not much is known about the ion channels and receptors involved in these effects. Thus, the impact of the sodium channel blocker carbamazepine, the calcium channel blocker flunarizine and the NMDA receptor antagonist dextromethorphane on tDCS-elicited motor cortical excitability changes of healthy human subjects were tested. tDCS-protocols inducing excitability alterations (1) only during tDCS and (2) eliciting long-lasting after-effects were applied after drug administration. Carbamazepine selectively eliminated the excitability enhancement induced by anodal stimulation during and after tDCS. Flunarizine resulted in similar changes. Antagonising NMDA receptors did not alter current-generated excitability changes during a short stimulation, which elicits no after-effects, but prevented the induction of long-lasting after-effects independent of their direction. These results suggest that, like in other animals, cortical excitability shifts induced during tDCS in humans also depend on membrane polarisation, thus modulating the conductance of sodium and calcium channels. Moreover, they suggest that the after-effects may be NMDA receptor dependent. Since NMDA receptors are involved in neuroplastic changes, the results suggest a possible application of tDCS in the modulation or induction of these processes in a clinical setting. The selective elimination of tDCS-driven excitability enhancements by carbamazepine proposes a role for this drug in focussing the effects of cathodal tDCS, which may have important future clinical applications."],["dc.identifier.doi","10.1113/jphysiol.2003.049916"],["dc.identifier.isi","000186990200026"],["dc.identifier.pmid","12949224"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44937"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.relation.issn","0022-3751"],["dc.title","Pharmacological modulation of cortical excitability shifts induced by transcranial direct current stimulation in humans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2007Journal Article
    [["dc.bibliographiccitation.firstpage","3807"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","3812"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Roth, Amelie"],["dc.contributor.author","Kuo, Min-Fang"],["dc.contributor.author","Fischer, Anja K."],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Lang, Nicolas"],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T11:03:16Z"],["dc.date.available","2018-11-07T11:03:16Z"],["dc.date.issued","2007"],["dc.description.abstract","Associative neuroplasticity, which encompasses the modification of synaptic strength by coactivation of two synaptic inputs, has been linked to learning processes. Because unlimited plasticity destabilizes neuronal networks, homeostatic rules were proposed and experimentally proven that control for the amount and direction of plasticity dependent on background network activity. Accordingly, low background activity would enhance facilitatory plasticity, whereas high background activity would inhibit it. However, the impact of background excitability on associative plasticity has not been studied so far in humans. Facilitatory associative plasticity was induced by paired associative stimulation (PAS) in the human motor cortex, whereas background activity was enhanced or diminished by transcranial direct current stimulation (tDCS). When applied before PAS, excitability-enhancing tDCS also boosted the efficacy of PAS, whereas excitability-diminishing tDCS turned it into inhibition. Thus, previous background activity does not influence associative plasticity homeostatically. When tDCS and PAS were applied simultaneously, now in accordance with homeostatic rules of neuroplasticity, reduced background activity resulted in a prolonged excitability enhancement by PAS, whereas enhanced background activity turned it into inhibition. We conclude that background network activity can influence associative plasticity homeostatically. However, only simultaneous modulation of both parameters is in accordance with homeostatic concepts. These findings might be of importance for the development of plasticity-inducing stimulation protocols supporting information processing in humans."],["dc.identifier.doi","10.1523/JNEUROSCI.5348-06.2007"],["dc.identifier.isi","000245468300022"],["dc.identifier.pmid","17409245"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51577"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Timing-dependent modulation of associative plasticity by general network excitability in the human motor cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2006Journal Article
    [["dc.bibliographiccitation.firstpage","1651"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","1657"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Nitsche, M. A."],["dc.contributor.author","Lampe, C."],["dc.contributor.author","Antal, Andrea"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Lang, N."],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T10:11:54Z"],["dc.date.available","2018-11-07T10:11:54Z"],["dc.date.issued","2006"],["dc.description.abstract","Dopaminergic mechanisms participate in N-methyl-D-aspartate (NMDA) receptor-dependent neuroplasticity, as animal experiments have shown. This may be similar in humans, where dopamine influences learning and memory. We tested the role of dopamine in human cortical neuroplasticity. Changes of excitability were induced by transcranial direct current stimulation (tDCS). D2 receptor blocking by sulpiride abolished the induction of after-effects nearly completely. D1 activation alone in the presence of D2 receptor blocking induced by co-administration of sulpiride and pergolide did not re-establish the excitability changes induced by tDCS. This suggests that D2 receptors play a major supporting role in inducing neuroplasticity in the human motor cortex. Enhancement of D2 and, to a lesser degree, D1 receptors by pergolide consolidated tDCS-generated excitability diminution until the morning after stimulation. The readiest explanation for this pattern of results is that D2 receptor activation has a consolidation-enhancing effect on tDCS-induced changes of excitability in the human cortex. The results of this study underscore the importance of the dopaminergic system for human neuroplasticity, suggest a first pharmacological add-on mechanism to prolong the excitability-diminishing effects of cathodal tDCS for up to 24 h after stimulation, and thus render the application of tDCS practicable in diseases displaying enhanced cortical excitability, e.g. migraine and epilepsy."],["dc.identifier.doi","10.1111/j.1460-9568.2006.04676.x"],["dc.identifier.isi","000236176000026"],["dc.identifier.pmid","16553629"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40135"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0953-816X"],["dc.title","Dopaminergic modulation of long-lasting direct current-induced cortical excitability changes in the human motor cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2002Journal Article
    [["dc.bibliographiccitation.firstpage","809"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuroreport"],["dc.bibliographiccitation.lastpage","811"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Sommer, M."],["dc.contributor.author","Lang, N."],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T10:29:53Z"],["dc.date.available","2018-11-07T10:29:53Z"],["dc.date.issued","2002"],["dc.description.abstract","In a blinded cross-over design, 10 healthy controls received 900 monophasic and biphasic repetitive transcranial magnetic stimuli over the primary motor cortex. Stimulation frequency was 1 Hz, and stimulation intensity 90% of the individual resting motor threshold. Suprathreshold stimuli applied at 0.1 Hz before and after repetitive stimulation controlled for changes in corticospinal excitability. We found a lasting corticospinal inhibition that was significantly more pronounced after monophasic than after biphasic repetitive transcranial magnetic stimulation (motor evoked potential amplitude reduced by 35 +/- 20% vs 12 +/- 37%, mean +/- s.d). We propose that the current flow in the coil plays a significant role in optimising after effects, and asymmetric current flow may be particularly efficient in building up tissue polarization. NeuroReport 13:809-811 (C) 2002 Lippincott Williams Wilkins."],["dc.identifier.doi","10.1097/00001756-200205070-00015"],["dc.identifier.isi","000175442400017"],["dc.identifier.pmid","11997692"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43739"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0959-4965"],["dc.title","Neuronal tissue polarization induced by repetitive transcranial magnetic stimulation?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2011Journal Article
    [["dc.bibliographiccitation.firstpage","2299"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cerebral Cortex"],["dc.bibliographiccitation.lastpage","2306"],["dc.contributor.author","Lang, Nicolas"],["dc.contributor.author","Rothkegel, Holger"],["dc.contributor.author","Reiber, Heidi"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Sueske, Elke"],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Wuttke, Wolfgang"],["dc.contributor.author","Paulus, Walter"],["dc.date.accessioned","2017-09-07T11:45:37Z"],["dc.date.available","2017-09-07T11:45:37Z"],["dc.date.issued","2011"],["dc.description.abstract","Circadian rhythms exert powerful influence on various aspects of human physiology and behavior. Here, we tested changes of human cerebral cortex excitability over the course of the day with transcranial magnetic stimulation (TMS). At different times of the day, intracortical and corticospinal excitability of the primary motor cortex (M1) was evaluated in 15 healthy subjects by TMS of left M1. While motor thresholds, short-interval intracortical inhibition and facilitation and input/output curves remained unchanged, we found that a specific form of γ-aminobutyric acid (GABA)–mediated intracortical inhibition, revealed by long-interval intracortical inhibition and cortical silent periods, progressively decreased during the course of the day. Additional experiments demonstrated that morning inhibition persisted irrespective of previous sleep or sleep deprivation. Corticotropin-releasing hormone (CRH) infusions in the evening lead to morning cortisol levels but did not restore levels of morning inhibition, whereas suppression of endogenous CRH release by repeated oral dexamethasone intake over 24 h prevented morning inhibition. The findings suggest a specific modulation of GABAergic motor cortex inhibition within the circadian cycle, possibly linked to the CRH system, and may indicate a neurobiological basis for variable neuroplasticity over the course of the day."],["dc.identifier.doi","10.1093/cercor/bhr003"],["dc.identifier.gro","3150416"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7178"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Circadian modulation of GABA-mediated cortical inhibition"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]
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  • 2006Journal Article
    [["dc.bibliographiccitation.firstpage","813"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.lastpage","819"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Lang, N."],["dc.contributor.author","Sueske, E."],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Tergau, Frithjof"],["dc.date.accessioned","2018-11-07T09:51:39Z"],["dc.date.available","2018-11-07T09:51:39Z"],["dc.date.issued","2006"],["dc.description.abstract","Purpose: To explore acute effects of pregabalin (PGB) on human motor cortex excitability with transcranial magnetic stimulation (TMS). Methods: PGB, 600 mg/day, was orally administered in 19 healthy subjects twice daily in a randomized, double-blind, placebo-controlled crossover design. Several measures of motor cortex excitability were tested with single- and paired-pulse TMS. Results: Mean short-interval intracortical inhibition (SICI) was reduced after PGB (74 +/- 7% of unconditioned response) compared with placebo (60 +/- 6% of unconditioned response). In contrast, mean long-interval intracortical inhibition (LICI) was increased by PGB (26 +/- 4% of unconditioned response) compared with placebo (45 +/- 8% of unconditioned response), and mean cortical silent period (CSP) showed an increase from 139 +/- 8 ms or 145 +/- 8 ms after placebo to 162 +/- 7 ms or 161 +/- 10 ms after PGB. Motor thresholds, intracortical facilitation, and corticospinal excitability were unaffected. Conclusions: The observed excitability changes with oppositional effects on SICI and LICI or CSP suggest gamma-aminobutyric acid (GABA)(B)-receptor activation. They are markedly distinct from those induced by gabapentin, although both PGB and gabapentin are thought to mediate their function by binding to the alpha(2)-delta subunit of voltage-gated calcium channels. Conversely, the TMS profile of PGB shows striking similarities with the pattern evoked by the GABA-reuptake inhibitor tiagabine."],["dc.identifier.doi","10.1111/j.1528-1167.2006.00544.x"],["dc.identifier.isi","000237350800002"],["dc.identifier.pmid","16686645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35957"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0013-9580"],["dc.title","Pregabalin exerts oppositional effects on different inhibitory circuits in human motor cortex: A double-blind, placebo-controlled transcranial magnetic stimulation study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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