Klinische Neurophysiologie 2012; 43 - V139
DOI: 10.1055/s-0032-1301524

Long-term and Time Dependent Homeostatic and Non-Homeostatic Metaplasticity in Human Motor Cortex

F Müller-Dahlhaus 1, C Möller 2, MK Lu 3, N Arai 4, A Fuhl 1, E Herrmann 5, U Ziemann 1
  • 1Universitätsklinikum Frankfurt am Main, Klinik für Neurologie, Frankfurt am Main
  • 2Klinik für Psychiatrie, Psychosomatik und Psychotherapie des Kindes- und Jugendalters, Frankfurt am Main
  • 3Department of Neurology, China Medical University Hospital, Taichung City, Taiwan
  • 4Department of Rehabilitation Medicine, Jikei University Aoto Hospital, Tokyo, Japan
  • 5Institut für Biostatistik und mathematische Modellierung, Frankfurt am Main

Aims: Studies in human primary motor cortex (M1) provided evidence for homeostatic as well as non-homeostatic forms of metaplasticity, but the conditions favoring one principle over the other are not well understood yet. Here we studied the role of time between two consecutive long-term potentiation (LTP)-like plasticity processes in human M1 on the expression of metaplasticity.

Methods: 27 healthy subjects participated in the study. Paired associative stimulation (PAS) was used to induce LTP-like plasticity in M1 (Müller-Dahlhaus et al. [2010] Front Synaptic Neurosci 2: 34). Motor cortical plasticity was indexed by the post/pre PAS ratio of motor evoked potential (MEP) amplitudes in resting abductor pollicis brevis muscle. We studied interactions between two consecutive PAS protocols (PAS1, PAS2) by testing a range of different inter-PAS intervals (10min, IPI10; 30min, IPI30; 60min, IPI60; 180min, IPI180).

Results: PAS1 induced similar LTP-like MEP increases in all experimental conditions. In contrast, PAS2 induced a significant further MEP increase at IPI30 only, notably with a longer time course as compared to PAS1 after-effects (non-homeostatic metaplasticity). This LTP-like plasticity after PAS2 at IPI30 was also present if MEPs were readjusted to baseline after PAS1 excluding changes in cortical excitability to underlie PAS2-induced LTP-like plasticity. Further analyses suggested homeostatic metaplasticity at IPI60 and IPI180, demonstrating time dependency of PAS1-PAS2 interactions. The cumulative PAS1 and PAS2 effect was significantly higher in the IPI30 condition than both the PAS1 effect alone and the cumulative PAS1 and PAS2 effect in all other conditions.

Conclusion: We conclude that LTP-like plasticity in human M1 is subject to long-term and time dependent metaplasticity. Findings imply that facilitation and incremental built-up of LTP-dependent processes in human M1 may be confined to specific time windows of (non-homeostatic) metaplasticity.