H. Hultborn et al., ON THE MECHANISM OF THE POST-ACTIVATION DEPRESSION OF THE H-REFLEX INHUMAN-SUBJECTS, Experimental Brain Research, 108(3), 1996, pp. 450-462
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.