Indeed, the main goal of homeostatic plasticity ERK inhibitor supplier studies is to control this directly by means of a ‘priming’ stimulus, as opposed to letting it vary normally, so as to optimize any effect of an intervention protocol (Fricke et al., 2011). The correlation between the change in the PPR and baseline state

was not evident in the measurement taken immediately after rTMS, although the average increase in the PPR even at that point was statistically significant. This is notable as it indicates that the influence of the baseline state of excitability on the response to rTMS is not present immediately after the stimulation has ended, but rather requires a time lapse to build up. This may indicate that the changes observed in the final measurement represent something closer to a ‘final’ size of response, before the effect begins to fade. However, this cannot be ascertained without a more prolonged period of post-stimulation testing. In the group that also received iHFS, this correlation between the baseline condition and the final measurement was not present, indicating that iHFS had a disruptive effect on the normal time course of the response to rTMS. It is important to note that, in the group that received rTMS alone (Group 2), the PPR

increased significantly after 25 min compared with the values obtained immediately after rTMS. This makes Crizotinib in vivo it unlikely that the lack of further increase in the PPR after iHFS in Group 1 was Tryptophan synthase simply due to a ceiling effect, as after rTMS the PPR value was almost identical for both groups. Furthermore, in the group that received iHFS alone (Group 3), the baseline value of the PPR approximated

the value found in the other two groups after rTMS. This did not prevent iHFS from producing a significant increase in the PPR, suggesting that the lack of effect of iHFS in Group 1 depended on the previous history of activity rather than on the value of the PPR at the time of stimulation. In contrast to the results obtained for cortical excitability, rTMS and iHFS showed no significant interaction in their effect on tactile acuity. Both groups experienced a significant improvement in two-point discrimination immediately following rTMS, which remained unchanged in the last assessment, with or without iHFS. A previous report, in which a similar rTMS protocol was used, also showed that the induced change in tactile acuity was strongest immediately after stimulation, and slowly reverted to baseline values over the following hours (Tegenthoff et al., 2005). This represents a marked difference from the effect of rTMS on cortical excitability, which, as was shown above, is considerably stronger 25 min after the end of stimulation than immediately after. In addition, the effect on the PPR was highly sensitive to iHFS, whereas iHFS had almost no influence on the rTMS-induced change in tactile acuity.