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Institute of Human Physiology, University of Genoa, Italy.

1. In standing subjects, toe-down rotation of a supporting platform elicits a medium-latency response (MLR) in tibialis anterior (TA) muscle and a long-latency response (LLR) in soleus (Sol). Toe-up rotation induces a short-latency response (SLR) in Sol and a LLR in TA. When subjects steadily hold onto a stable frame, all responses are decreased, except Sol SLR. The aim of this investigation was to assess whether the response modulation is dependent on information from the hand touching the frame, or whether it anticipates the holding task. 2. The time course of the changes in response amplitude was studied in a time interval centred around the act of holding, performed in a reaction-time mode. Subjects kept their extended arm close to the frame in front of them and brought the hand in contact with the frame in response to a visual go-signal. The platform was moved at different intervals prior to or after the go-signal. Surface EMGs of Sol, TA and deltoid (Delt) were recorded. 3. TA MLR began to decrease when the platform was displaced at an interval of 140 ms after the go-signal, about 200 ms before subjects touched the frame and 120 ms before termination of Delt EMG. Four hundred milliseconds after the go-signal the response reached and maintained maximal inhibition, similar to that occurring under the stationary holding condition. The time course of inhibition of Sol LLR and TA LLR was similar to that of TA MLR, except that LLRs began to decrease at an earlier interval. Due to the different response latency from the onset of the perturbations, the beginning of inhibition of both MLRs and LLRs occurred almost simultaneously. 4. The changes in amplitude of leg muscle responses are not triggered by the go-signal, contact with the frame, or arm motion, suggesting that the modulation is related to the transition to a new, stabilized postural 'set'. The similar extent and parallel time course of MLR and LLR suppression, possibly transmitted through different pathways, points to the spinal cord as the site of action. The lack of depression of the monosynaptic SLR suggests an effect at premotoneuronal level. On the basis of selectivity, latency and time course of the effect, we favour the hypothesis that a monoaminergic pathway from the brainstem is involved.

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