2001; Radovanovic et al. 2002). Furthermore, our time course of SMA activity was similar to that elicited by median nerve stimulation and PM using EEG and electrocorticography. We located the source of activity in the posterior wall of the postcentral fissure 64–114 msec following PM, and this ECD location was 23.8 mm posterior, 19.3 mm medial,

and 9.0 mm superior to the source estimated at N20m. Using BESA analysis, Hoshiyama et al. (1997b) reported that the ECD location of PPC was 24 mm posterior, 19 mm medial, and 26 mm superior to the Inhibitors,research,lifescience,medical S1 hand area (Hoshiyama et al. 1997b). Areas 5 and 7 in the posterior wall of the postcentral fissure are considered to be at a higher level than S1 in the processing of somatic information (Duffy and Burchfiel 1971; Sakata et al. 1973; MacKay et al. 1978). Prevosto et al. (2011) identified direct and polysynaptic somatosensory pathways from areas 2 Inhibitors,research,lifescience,medical and 3a to PPC, and they found that PPC receives disynaptic inputs from dorsal column nuclei as directly as other somatosensory areas (Prevosto et al. 2011). EEG (Arezzo et al. 1981), PET (Radovanovic et al. 2002), and fMRI (Albanese et al. 2009) studies have also reported that neurons in areas 5 and 7 are activated

by PMs. The PPC is most active 70–110 msec after median nerve stimulation (Forss et al. 1994; Mauguiere Inhibitors,research,lifescience,medical et al. 1997). In this present study, we have confirmed the activities in PPC and the time course of PPC activity with regard to passive finger movement using MEG. We have also elucidated the activities of S2 areas following PM over the hemispheres contralateral (n = 7) and/or ipsilateral Inhibitors,research,lifescience,medical (n = 7) to the movement, with these activities peaking approximately 120 msec after the onset of PM. There have been many MEG studies of S2 activities following electrical stimulation (Forss et al. 1994; Mima et al. 1998; Hari and Forss 1999), mechanical stimulation (Hoechstetter et al. 2000, 2001; Onishi et al. 2010), and PM (Xiang et al. 1997; Alary et al. 2002). MEG responses from S2 were

LGK-974 chemical structure bilateral and peaked at Inhibitors,research,lifescience,medical 80–150 msec (Forss and Jousmaki 1998). Our results of bilateral S2 responses agree with those of previous reports. We could not observe MEF with a latency of >150 msec (MEF2) in this study, although MEF2 has been recorded 150–200 msec after the onset of active movement either in previous studies (Nagamine et al. 1994; Hoshiyama et al. 1997a; Kristeva-Feige et al. 1997; Cheyne et al. 2006). In addition, we have shown no evidence of activities in SMA and S2 after voluntary movements, although many researchers have reported that active movement is associated with activation of SMA and bilateral S2 areas using fMRI or PET (Rao et al. 1993; Weiller et al. 1996; Mima et al. 1999a). Here, the participants were instructed to maintain the MP joint at the extension position for a moment. As a result, muscle activity continued for >500 msec after movement onset. Consequently, neurons in area 4 remained active during this time to hold the muscle contraction.