Post-activation depression of primary afferents reevaluated in humans.

Amplitude variation of Hoffmann Reflex (H-reflex) was used as a tool to investigate many neuronal networks. However, H-reflex itself is a subject to intrinsic changes including post-activation depression (P-AD). We aimed to investigate P-AD and its implication on motor control in humans. Upon tibial nerve stimulation in 23 healthy participants, peak-to-peak amplitude change of H-reflex was investigated using surface electromyography (SEMG) of soleus muscle. Variety of stimulus intensities, interstimulus intervals (ISIs), voluntary contraction levels/types and force recording were used to investigate the nature of P-AD. We have shown that P-AD was significantly stronger in the shorter ISIs. The only exception was the ISI of 200 msecs which had a weaker P-AD than some of the longer ISIs. Sudden muscle relaxation, on the other hand, further increased the effectiveness of the ongoing P-AD. Moreover, P-AD displayed its full effect with the first stimulus when there was no muscle contraction and was efficient to reduce the muscle force output by about 30%. These findings provide insight about the variations and mechanism of P-AD and could lead to improvements in diagnostic tools in neurological diseases.

Transcranial magnetic stimulation induced early silent period and rebound activity re-examined.

Despite being widely studied, the underlying mechanisms of transcranial magnetic brain stimulation (TMS) induced motor evoked potential (MEP), early cortical silent period (CSP) and rebound activity are not fully understood. Our aim is to better characterize these phenomena by combining various analysis tools on firing motor units. Responses of 29 tibialis anterior (TA) and 8 abductor pollicis brevis (APB) motor units to TMS pulses were studied using discharge rate and probability-based tools to illustrate the profile of the synaptic potentials as they develop on motoneurons in 24 healthy volunteers. According to probability-based methods, TMS pulse produces a short-latency MEP which is immediately followed by CSP that terminates at rebound activity. Discharge rate analysis, however, revealed not three, but just two events with distinct time courses; a long-lasting excitatory period (71.2 ± 9.0 ms for TA and 42.1 ± 11.2 ms for APB) and a long-latency inhibitory period with duration of 57.9 ± 9.5 ms for TA and 67.3 ± 13.8 ms for APB. We propose that part of the CSP may relate to the falling phase of net excitatory postsynaptic potential induced by TMS. Rebound activity, on the other hand, may represent tendon organ inhibition induced by MEP activated soleus contraction and/or long-latency intracortical inhibition. Due to generation of field potentials when high intensity TMS is used, this study is limited to investigate the events evoked by low intensity TMS only and does not provide information about later parts of much longer CSPs induced by high intensity TMS. Adding discharge rate analysis contributes to obtain a more accurate picture about the characteristics of TMS-induced events. These results have implications for interpreting motor responses following TMS for diagnosis and overseeing recovery from various neurological conditions.