, 2011). The fast signal depends, at least Etoposide mw partially, on spiking activity, as tetrodoxin (TTX) dampens the oscillations (Welsh et al., 2010). A surprising datum of Hong et al. (in press) is that TTX induced oscillations in some cells

that were formerly silent. This suggests that some spike-dependent inhibitory influence is removed by TTX, a problem for further investigation. What is also not yet clear is the mechanistic basis for the slow spread of signal from one region to the next. Hong et al. (in press) implicate a calcium wave and future work will show whether calcium is a primary player, or perhaps it shares the spotlight with other ions or small molecules mediating slow signal spread. “
“Placebos have been found to affect a number of pathological processes and physiological functions through

selleck expectations of clinical improvement. Recently, the study of the placebo effect has moved from the clinical to the physical performance setting, wherein placebos can boost performance by increasing muscle work and by decreasing perceived exertion. However, nothing is known about the neurobiological underpinnings of this phenomenon. Here we show for the first time that a placebo, which subjects believed to be endurance-increasing caffeine, reduces fatigue by acting at the central level on the preparatory phase of movement. In fact, we recorded the readiness potential, which is the expression of the preparatory phase of movement at the level of the supplementary motor area, during repeated flexions of the index finger in a control group that did not receive any treatment and in a placebo group that received placebo caffeine. In the control group, as the number of flexions increased, both fatigue and readiness potential amplitude increased. By contrast, in the placebo group, as the number of flexions increased we found a decrease in perceived exertion along with no increase in readiness potential amplitude. This placebo-induced modulation of the readiness potential suggests that placebos reduce fatigue by acting centrally during the anticipatory phase of movement, thus emphasizing only the important

role of the central nervous system in the generation of fatigue. “
“The amplitudes of auditory evoked N1 m responses are known to depend on the length of the pre-stimulus silent interval. However, it remains unknown whether pre-penultimate silent intervals affect the auditory evoked responses elicited by test stimuli. In the present study, we investigated the N1 m responses elicited by a train of four successive tones with a silent interval of 1 s subsequent to that with a 0.25-, 0.5-, 2- or 4-s silent interval using magnetoencephalography. The results obtained demonstrated that the N1 m source strength decreased as the pre-penultimate silent interval became shorter. A history of silences had a significant impact on the N1 m source strength.