Facilitation and inhibition of tibialis anterior responses to corticospinal stimulation after maximal voluntary contractions.

نویسندگان

  • Sabine Giesebrecht
  • Peter G Martin
  • Simon C Gandevia
  • Janet L Taylor
چکیده

The corticospinal pathway is the major pathway controlling human voluntary movements. After strong voluntary contractions, the efficacy of corticospinal transmission to elbow flexors is reduced for approximately 90 s, and this limits motoneuronal output. This reduction may reflect activity-dependent changes at cortico-motoneuronal synapses. We investigated whether similar changes occur in a leg muscle, tibialis anterior (TA). Electrical stimuli over high thoracic vertebrae activated corticospinal axons to evoke an EMG response in TA (TMEP). Stimuli were delivered before and after short 10-s and prolonged 1-min maximal contractions (MVCs) of ankle dorsiflexors. In two studies, stimuli were given with the muscle relaxed. In other studies, stimuli were given during weak contraction. After a 10-s MVC (study 1, n = 10), TMEPs increased immediately to 349 +/- 335% (mean +/- SD) of control values. By 1 min after contraction, TMEPs decreased to 38 +/- 28% of control and remained depressed for >10 min. Facilitation (191 +/- 133% control) and depression (18 +/- 22% control) occurred over the same time course after the 1-min MVC (study 2, n = 10). When tested during weak contraction (study 3, n = 10), TMEPs showed less facilitation (131 +/- 41% control) and less depression (67 +/- 21% control) and responses returned to baseline over approximately 15 min. In contrast to TMEPs, H-reflexes in TA were little changed after a 10-s MVC (study 4, n = 7). Our findings reveal an immediate facilitation and subsequent longer-lasting depression in corticospinal transmission to TA, which originate at a premotoneuronal site. This behavior differs markedly from that in elbow flexor muscles and suggests that activity-dependent changes in the motor pathway may be muscle specific.

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عنوان ژورنال:
  • Journal of neurophysiology

دوره 103 3  شماره 

صفحات  -

تاریخ انتشار 2010