ON THE MECHANISM OF THE POST-ACTIVATION DEPRESSION OF THE H-REFLEX INHUMAN-SUBJECTS

It was demonstrated that the soleus H-reflex was depressed for more th an 10 s following a preceding passive dorsiflexion of the ankle joint. This depression was caused by activation of large-diameter afferents with receptors located in the leg muscles, as an ischaemic block of la rge-diameter fibres just below the knee joint abolished the depression , whereas a similar block just proximal to the ankle joint was ineffec tive. The depression of the H-reflex was not caused by changes in moto neuronal excitability, as motor-evoked potentials by magnetic brain st imulation were not depressed by the same passive dorsiflexion. Therefo re it was concluded that the long-lasting depression is due to mechani sms acting at presynaptic level. The transmission of the monosynaptic Ia excitation from the femoral nerve to soleus motoneurones was not de pressed by the ankle dorsiflexion. The depression thus seems to be con fined to those afferents that were activated by the conditioning dorsi flexion. In parallel experiments on decerebrate cats, more invasive me thods have complemented the indirect techniques used in the experiment s on human subjects. A similar long-lasting depression of triceps sura e monosynaptic reflexes was evoked by a preceding conditioning stimula tion of the triceps surae Ia afferents. This depression was accompanie d by a reduction of the monosynaptic Ia excitatory postsynaptic potent ial recorded intracellularly in triceps surae motoneurones, but not by changes in the input resistance or membrane potential in the motoneur ones. Stimulation of separate branches within the triceps surae nerve demonstrated that the depression is confined to those afferents that w ere activated by the conditioning stimulus. This long-lasting depressi on was not accompanied by a dorsal root potential. It is concluded tha t the long-lasting depression is probably caused by a presynaptic effe ct, but different from the ''classical'' GABAergic presynaptic inhibit ion which is widely distributed among afferent fibres and accompanied by dorsal root potentials. It is more probably related to the phe nome non of a reduced transmitter release from previously activated fibres, i.e. a homosynaptic post-activation depression. The consequences of t his post-activation depression for the interpretation of results on sp inal mechanisms during voluntary movements in man are discussed.