Learning Modifies Subsequent Induction of Long-Term Potentiation-Like and Long-Term Depression-Like Plasticity in Human Motor Cortex

Ziemann, Ulf; Iliać, Tihomir V.; Pauli, Christian; Meintzschel, Frank; Ruge, Diane

doi:10.1523/jneurosci.5016-03.2004

Cited by 531 publications

(557 citation statements)

References 37 publications

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“…This LTP-like increase in MEP amplitude shows tight similarities to cellular LTP because it is associative, input specific, and blocked by dextromethorphan, a non-competitive NMDAR antagonist (Stefan et al, 2002;Stefan et al, 2000;Wolters et al, 2003). Furthermore, PAS LTP -induced LTP-like plasticity interacts homeostatically with prior or subsequent motor learning (Elahi et al, 2013;Jung and Ziemann, 2009;Kang et al, 2011;Rosenkranz et al, 2007;Stefan et al, 2006;Ziemann et al, 2004), indicating its mechanistic importance in learning processes.…”

Section: Introductionmentioning

confidence: 77%

“…In slice preparations of rat motor cortex (M1), LTP induction depends on disinhibition by application of a synaptic GABAAR antagonist and can be disrupted by NMDAR blockade (Aroniadou and Keller, 1995;Castro-Alamancos et al, 1995;Fritsch et al, 2010;Hess et al, 1996). At the systems level of human M1, LTP-like plasticity, indexed by a long-term increase in motor-evoked potential (MEP) amplitude, can be induced by paired associative stimulation (PAS LTP ) (Cooke and Bliss, 2006;Müller-Dahlhaus et al, 2010;Stefan et al, 2002;Stefan et al, 2000;Ziemann et al, 2004). This LTP-like increase in MEP amplitude shows tight similarities to cellular LTP because it is associative, input specific, and blocked by dextromethorphan, a non-competitive NMDAR antagonist (Stefan et al, 2002;Stefan et al, 2000;Wolters et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Lücke

Heidegger

Röhner

et al. 2014

Neuropsychopharmacol

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Ingesting ethanol (EtOH) at low doses during social drinking is a common human behavior for its facilitating effects on social interactions. However, low-dose EtOH may have also detrimental effects that so far are underexplored. Here we sought to test the effects of lowdose EtOH on long-term potentiation (LTP)-like plasticity in human motor cortex. Previous cellular experiments showed that low-dose EtOH potentiates extrasynaptic GABAAR and reduces NMDAR-mediated currents, processes that would limit the expression of LTP. Paired associative transcranial magnetic stimulation (PAS LTP ) was employed in nine healthy subjects for induction of LTP-like plasticity, indexed by a long-term increase in motor-evoked potential input-output curves. Synaptic a1-GABAAR function was measured by saccadic peak velocity (SPV). Very low doses of EtOH (resulting in blood concentrations of o5 mM) suppressed LTP-like plasticity but did not affect SPV when compared with a placebo condition. In contrast, 1 mg of alprazolam, a classical benzodiazepine, or 10 mg of zolpidem, a non-benzodiazepine hypnotic, decreased SPV but did not significantly affect LTP-like plasticity when compared with placebo. This double dissociation of low-dose EtOH vs alprazolam/zolpidem effects is best explained by the putatively high affinity of EtOH but not alprazolam/zolpidem to extrasynaptic GABAARs and to NMDARs. Findings suggest that enhancement of extrasynaptic GABAARmediated tonic inhibition and/or reduction of NMDAR-mediated neurotransmission by EtOH blocks LTP-like plasticity in human cortex at very low doses that are easily reached during social drinking. Therefore, low-dose EtOH may jeopardize LTP-dependent processes, such as learning and memory formation.

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Section: Introductionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Lücke

Heidegger

Röhner

et al. 2014

Neuropsychopharmacol

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show abstract

“…Although both healthy and depressed subjects showed significant improvement in the rotor pursuit task, motor learning was comparatively impaired in depressed subjects. The lack of correlation between motor learning and PAS test results may be considered surprising as motor learning is considered at least partially reliant on LTP in the primary motor cortex (Ziemann et al, 2004). However, very few studies have found a significant relationship between motor learning outcomes and results of brain stimulation tests of motor cortex plasticity.…”

Section: Discussionmentioning

confidence: 99%

Neuroplasticity in Depressed Individuals Compared with Healthy Controls

Player

Taylor

Weickert

et al. 2013

Neuropsychopharmacol

106

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Several lines of evidence suggest that neuroplasticity is impaired in depression. This study aimed to compare neuroplasticity in 23 subjects with DSM-IV major depressive episode and 23 age-and gender-matched healthy controls, using an objective test that is independent of subject effort and motivation. Neuroplasticity was assessed in the motor cortex using a brain stimulation paradigm known as paired associative stimulation (PAS), which induces transient changes in motor cortical function. Motor cortical excitability was assessed before and after PAS using single-pulse transcranial magnetic stimulation (TMS) to induce motor evoked potentials (MEPs) in a hand muscle. After PAS, MEP amplitudes significantly increased in healthy controls compared with depressed subjects (P ¼ 0.002). The functional significance of motor cortical changes was assessed using a motor learning task-a computerized version of the rotor pursuit task. Healthy controls also performed better on motor learning (P ¼ 0.02). BDNF blood levels and genotype were assayed to determine any relationship with motor cortical plasticity. However, PAS results did not correlate with motor learning, nor appear to be related to BDNF measures. The significance of these findings is that it provides one of the first direct demonstrations of reduced neuroplasticity in depressed subjects, using an objective test.

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“…Research has suggested that repeated sessions of NIBS can increase the duration of the effects (Nyffeler et al, 2006;Meinzer et al, 2014). However, repeated plasticity-inducing paradigms can also attenuate the effects of subsequent stimulation (Ziemann et al, 2004). In this context, synaptic connections potentiated by the initial plasticity paradigm are rendered less able to do so with subsequent stimulation (indeed the synaptic connections become more responsive to inhibitory paradigms -a concept referred to as metaplasticity (Turrigiano, 1999)).…”

Section: Other Considerationsmentioning

confidence: 99%

Imaging human brain networks to improve the clinical efficacy of non-invasive brain stimulation

Sale¹,

Mattingley²,

Zalesky³

et al. 2015

Neuroscience & Biobehavioral Reviews

127

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Learning Modifies Subsequent Induction of Long-Term Potentiation-Like and Long-Term Depression-Like Plasticity in Human Motor Cortex

Cited by 531 publications

References 37 publications

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Neuroplasticity in Depressed Individuals Compared with Healthy Controls

Imaging human brain networks to improve the clinical efficacy of non-invasive brain stimulation

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