Loss of topographic specificity of LTD-like plasticity is a trait marker in focal dystonia

Weise, David; Schramm, Axel; Beck, Manfred; Reiners, Karlheinz; Claßen, Joseph

doi:10.1016/j.nbd.2010.11.009

Cited by 40 publications

(41 citation statements)

References 41 publications

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“…These results suggest that focal hand dystonia is associated with a dysfunctional homeostatic regulation of plasticity, which might set the frame for aberrant sensorimotor plasticity. Indeed, several NTBS studies have shown that patients with focal hand dystonia show excessive sensorimotor plasticity with lack of somatotopic specificity [129,130]. It should be noted though that focal dystonia is also characterized by deficient inhibition within intracortical circuits [131].…”

Section: Focal Dystoniamentioning

confidence: 99%

Consensus Paper: Probing Homeostatic Plasticity of Human Cortex With Non-invasive Transcranial Brain Stimulation

et al. 2015

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Homeostatic plasticity is thought to stabilize neural activity around a set point within a physiologically reasonable dynamic range. Over the last ten years, a wide range of non-invasive transcranial brain stimulation (NTBS) techniques have been used to probe homeostatic control of cortical plasticity in the intact human brain. Here, we review different NTBS approaches to study homeostatic plasticity on a systems level and relate the findings to both, physiological evidence from in vitro studies and to a theoretical framework of homeostatic function. We highlight differences between homeostatic and other non-homeostatic forms of plasticity and we examine the contribution of sleep in restoring synaptic homeostasis. Finally, we discuss the growing number of studies showing that abnormal homeostatic plasticity may be associated to a range of neuropsychiatric diseases.

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Section: Focal Dystoniamentioning

confidence: 99%

Consensus Paper: Probing Homeostatic Plasticity of Human Cortex With Non-invasive Transcranial Brain Stimulation

et al. 2015

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“…It has also been shown that an ISI of 21.5 ms may have similar effects (Weise et al, 2006, 2011). Such increases can however also be obtained when a fixed inter-stimulus interval (ISI) of 35 ms is employed (Stefan et al, 2000).…”

Section: Timing Dependency In Pasmentioning

confidence: 88%

“…In order to induce LTD-type effects in corticospinal projections to the hand (Table 2), it has been customary to employ a fixed ISI of 10 ms (“PAS10”), with a view to ensuring that a corollary of the afferent volley arrives at M1 after the magnetic cortical stimulus (e.g., Wolters et al, 2003; Monte-Silva et al, 2009; Thirugnanasambandam et al, 2011a,b; Weise et al, 2011). In a recent study however, Schabrun et al (2013) reported that MEP amplitudes were reduced by a PAS protocol in which electrical stimulation of the median nerve was applied at fixed intervals of 250, 350, and 450 ms following the delivery of TMS to contralateral M1.…”

Section: Timing Dependency In Pasmentioning

confidence: 99%

Modulation of human corticospinal excitability by paired associative stimulation

Carson

Kennedy

2013

Front. Hum. Neurosci.

131

141

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Paired Associative Stimulation (PAS) has come to prominence as a potential therapeutic intervention for the treatment of brain injury/disease, and as an experimental method with which to investigate Hebbian principles of neural plasticity in humans. Prototypically, a single electrical stimulus is directed to a peripheral nerve in advance of transcranial magnetic stimulation (TMS) delivered to the contralateral primary motor cortex (M1). Repeated pairing of the stimuli (i.e., association) over an extended period may increase or decrease the excitability of corticospinal projections from M1, in manner that depends on the interstimulus interval (ISI). It has been suggested that these effects represent a form of associative long-term potentiation (LTP) and depression (LTD) that bears resemblance to spike-timing dependent plasticity (STDP) as it has been elaborated in animal models. With a large body of empirical evidence having emerged since the cardinal features of PAS were first described, and in light of the variations from the original protocols that have been implemented, it is opportune to consider whether the phenomenology of PAS remains consistent with the characteristic features that were initially disclosed. This assessment necessarily has bearing upon interpretation of the effects of PAS in relation to the specific cellular pathways that are putatively engaged, including those that adhere to the rules of STDP. The balance of evidence suggests that the mechanisms that contribute to the LTP- and LTD-type responses to PAS differ depending on the precise nature of the induction protocol that is used. In addition to emphasizing the requirement for additional explanatory models, in the present analysis we highlight the key features of the PAS phenomenology that require interpretation.

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“…10 ms interval – PAS 10 ), excitability decreases [18]. Secondly, the change in excitability is specific to the cortical representation of the stimulated cutaneous region [17]–[19]. Thirdly, both LTP-like and LTD-like plasticity is likely mediated by synapses of excitatory neurons [20], [21] and cannot be induced if NMDA receptors are blocked [18], [22].…”

Section: Introductionmentioning

confidence: 99%

Altered Synaptic Plasticity in Tourette's Syndrome and Its Relationship to Motor Skill Learning

Brandt

Niessen²,

Ganos

et al. 2014

PLoS ONE

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Gilles de la Tourette syndrome is a neuropsychiatric disorder characterized by motor and phonic tics that can be considered motor responses to preceding inner urges. It has been shown that Tourette patients have inferior performance in some motor learning tasks and reduced synaptic plasticity induced by transcranial magnetic stimulation. However, it has not been investigated whether altered synaptic plasticity is directly linked to impaired motor skill acquisition in Tourette patients. In this study, cortical plasticity was assessed by measuring motor-evoked potentials before and after paired associative stimulation in 14 Tourette patients (13 male; age 18–39) and 15 healthy controls (12 male; age 18–33). Tic and urge severity were assessed using the Yale Global Tic Severity Scale and the Premonitory Urges for Tics Scale. Motor learning was assessed 45 minutes after inducing synaptic plasticity and 9 months later, using the rotary pursuit task. On average, long-term potentiation-like effects in response to the paired associative stimulation were present in healthy controls but not in patients. In Tourette patients, long-term potentiation-like effects were associated with more and long-term depression-like effects with less severe urges and tics. While motor learning did not differ between patients and healthy controls 45 minutes after inducing synaptic plasticity, the learning curve of the healthy controls started at a significantly higher level than the Tourette patients' 9 months later. Induced synaptic plasticity correlated positively with motor skills in healthy controls 9 months later. The present study confirms previously found long-term improvement in motor performance after paired associative stimulation in healthy controls but not in Tourette patients. Tourette patients did not show long-term potentiation in response to PAS and also showed reduced levels of motor skill consolidation after 9 months compared to healthy controls. Moreover, synaptic plasticity appears to be related to symptom severity.

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Loss of topographic specificity of LTD-like plasticity is a trait marker in focal dystonia

Cited by 40 publications

References 41 publications

Consensus Paper: Probing Homeostatic Plasticity of Human Cortex With Non-invasive Transcranial Brain Stimulation

Consensus Paper: Probing Homeostatic Plasticity of Human Cortex With Non-invasive Transcranial Brain Stimulation

Modulation of human corticospinal excitability by paired associative stimulation

Altered Synaptic Plasticity in Tourette's Syndrome and Its Relationship to Motor Skill Learning

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