On the mechanism of the post-activation depression of the H-reflex in human subjects

Abstract

It was demonstrated that the soleus H-reflex was depressed for more than 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 large-diameter fibres just below the knee joint abolished the depression, whereas a similar block just proximal to the ankle joint was ineffective. The depression of the H-reflex was not caused by changes in motoneuronal excitability, as motor-evoked potentials by magnetic brain stimulation were not depressed by the same passive dorsiflexion. Therefore it was concluded that the long-lasting depression is due to mechanisms acting at presynaptic level. The transmission of the monosynaptic Ia excitation from the femoral nerve to soleus motoneurones was not depressed by the ankle dorsiflexion. The depression thus seems to be confined to those afferents that were activated by the conditioning dorsiflexion. In parallel experiments on decerebrate cats, more invasive methods have complemented the indirect techniques used in the experiments on human subjects. A similar long-lasting depression of triceps surae monosynaptic reflexes was evoked by a preceding conditioning stimulation of the triceps surae Ia afferents. This depression was accompanied by a reduction of the monosynaptic Ia excitatory postsynaptic potential recorded intracellularly in triceps surae motoneurones, but not by changes in the input resistance or membrane potential in the motoneurones. Stimulation of separate branches within the triceps surae nerve demonstrated that the depression is confined to those afferents that were activated by the conditioning stimulus. This long-lasting depression was not accompanied by a dorsal root potential. It is concluded that the long-lasting depression is probably caused by a presynaptic effect, but different from the "classical" GABAergic presynaptic inhibition which is widely distributed among afferent fibres and accompanied by dorsal root potentials. It is more probably related to the phenomenon of a reduced transmitter release from previously activated fibres, i.e. a homosynaptic post-activation depression. The consequences of this post-activation depression for the interpretation of results on spinal mechanisms during voluntary movements in man are discussed.

Characteristics of preceding Ia activity on postactivation depression in health and disease

“…None of these possibilities are mutually exclusive. Although it was suggested in the 1960s that PAD activates long loop reflexes (Taborikova and Sax 1969), later intracellular experiments suggested that this type of inhibition does not spread to other Ia fibers (Hultborn et al 1996). Regardless of the physiological reason for this phenomenon, we established normative data to compare with the pathological condition.…”

“…Furthermore, PAD does not interfere with heteronymous sources to the motor pool (Beswick and Evanson 1957). Hultborn et al (1996) demonstrated that this presynaptic inhibitory mechanism is not accompanied by GABAergic primary afferent depolarization and does not produce dorsal root potentials. They also concluded that this inhibition does not spread to the motoneuron pool and is strictly confined to those Ia fibers that have been previously activated.…”

Changes in Segmental and Motor Cortical Output With Contralateral Muscle Contractions and Altered Sensory Inputs in Humans

“…Changes of such long duration have not previously been described. Postactivation depression is of longer duration than axo-axonal presynaptic inhibition but has still largely recovered in 10 s (Crone and Nielsen 1989;Hultborn et al 1996). Furthermore, this type of presynaptic depression is homosynaptic.…”

Effects of sustained stimulation on the excitability of motoneurons innervating paralyzed and control muscles

“…Moreover, postactivation homosynaptic depression of Ia afferents occurs with 18-Hz stimulation (e.g., Refs. 3,18), so this should markedly diminish reflex activation of the motoneurons by these afferents. Similar processes probably occur in other large-diameter afferents.…”