The study aims to investigate the after-effect of three sessions of intermittent theta-burst stimulation (iTBS) on motor cortical excitability. The iTBS was induced over the primary motor cortex (M1) at different time intervals. Methods: The study has a crossover design. Sixteen participants were assigned to three groups and received different accelerated iTBS (aiTBS) protocols during each visit: (1) three continuous sessions with no interval (iTBS18000); (2) three iTBS sessions with 10-min intervals (iTBS600 × 3 * 10); and (3) three iTBS sessions with 30-min intervals (iTBS600 × 3 * 30). As washout period, each visit is separated by at least 7 days. We measured the motor cortical excitability changes and intracortical inhibition. Results: A dose of 1,800 pulses of aiTBS per day is tolerable. The iTBS1800 led to a reduced cortical excitability; whereas iTBS600 × 3 * 10 and iTBS600 × 3 * 30 enhanced cortical excitability to a differential extent. After a total dose of 1,800 pulses, iTBS600 × 3 * 30 exhibited the longer effect and highest percentage of individuals with enhanced cortical excitability. Conclusion: The results suggest that aiTBS protocols at different time intervals result in different motor cortical excitability after-effects.

Sleep is essential in maintaining physiological homeostasis in the brain. While the underlying mechanism is not fully understood, a 'synaptic homeostasis' theory has been proposed that synapses continue to strengthen during awake, and undergo downscaling during sleep. This theory predicts that brain excitability increases with sleepiness. Here, we collected transcranial magnetic stimulation (TMS) measurements in 38 subjects in a 34-hour program, and decoded the relationship between cortical excitability and self-report sleepiness using advanced statistical methods. By utilizing a combination of partial least squares (PLS) regression and mixed-effect models, we identified a robust pattern of excitability changes, which can quantitatively predict the degree of sleepiness. Moreover, we found that synaptic strengthen occurred in both excitatory and inhibitory connections after sleep deprivation. In sum, our study provides supportive evidence for the synaptic homeostasis theory in human sleep and clarifies the process of synaptic strength modulation during sleepiness.

No abstract