Article

Time course of the induction of homeostatic plasticity generated by repeated transcranial direct current stimulation (tDCS) of the human motor cortex

Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College of London, London, United Kingdom.
Journal of Neurophysiology (Impact Factor: 2.89). 12/2010; 105(3):1141-9. DOI: 10.1152/jn.00608.2009
Source: PubMed

ABSTRACT

Several mechanisms have been proposed that control the amount of plasticity in neuronal circuits and guarantee dynamic stability of neuronal networks. Homeostatic plasticity suggests that the ease with which a synaptic connection is facilitated/suppressed depends on the previous amount of network activity. We describe how such homeostatic-like interactions depend on the time interval between two conditioning protocols and on the duration of the preconditioning protocol. We used transcranial direct current stimulation (tDCS) to produce short-lasting plasticity in the motor cortex of healthy humans. In the main experiment, we compared the aftereffect of a single 5-min session of anodal or cathodal tDCS with the effect of a 5-min tDCS session preceded by an identical 5-min conditioning session administered 30, 3, or 0 min beforehand. Five-minute anodal tDCS increases excitability for about 5 min. The same duration of cathodal tDCS reduces excitability. Increasing the duration of tDCS to 10 min prolongs the duration of the effects. If two 5-min periods of tDCS are applied with a 30-min break between them, the effect of the second period of tDCS is identical to that of 5-min stimulation alone. If the break is only 3 min, then the second session has the opposite effect to 5-min tDCS given alone. Control experiments show that these shifts in the direction of plasticity evolve during the 10 min after the first tDCS session and depend on the duration of the first tDCS but not on intracortical inhibition and facilitation. The results are compatible with a time-dependent "homeostatic-like" rule governing the response of the human motor cortex to plasticity probing protocols.

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    • "Animal studies with a higher current density of 25 mA/cm 2 did not induce lesions in the brain tissue, meaning that limits well above those applied in humans did not result in potential adverse effects[10], thereby demonstrating that it is a safe technique. There is evidence that repeated sessions of tDCS may be associated with a longer duration of the behavioral ef- fects[11]. Monte-Silva et al.[12]demonstrated that the interval between the sessions can be critical to performance . The authors found that when an extra session of tDCS is applied for 1 hour after the first session, the effects last for a longer time (120 minutes) compared to the effect of only one or two consecutive sessions, while an extra session of tDCS applied beyond that period (that is, 3 hours) did not influence the effect of the first session. "
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    • "These lasting effects cannot be explained as persistent network activity in the absence of some adaptive process since in our previous work gamma power returned to baseline activity within 100 ms after short-lasting DC field stimulation (Reato et al. 2010). Importantly, the afterstimulation effect was consistent with the acute effect, reminiscent of Hebbian or activitydependent plasticity and contrary to homeostatic plasticity (Fricke et al. 2011; Reato et al. 2013). "
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    • "In particular, NMDA and AMPA receptors are essential for synaptic plasticity by influencing long-term potentiation and depression (LTP and LTD) across structurally-connected brain regions (Bliss and Collingridge, 1993). These synaptic and neuronal pathways consolidate into stable and long-lasting functional brain networks (Fricke et al., 2011; Venkatakrishnan et al., 2011; Venkatakrishnan and Sandrini, 2012). However, the effects of tDCS on glutamate levels and its relation to largescale network connectivity have yet to be fully elucidated; that is, there must be a better understanding of how tDCS interacts across different scales within the brain's neural architecture by combining different, yet complementary, imaging modalities (see Hunter et al., 2013 for a review), which was the primary objective of the present study. "
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