Y. Chaix et al., FURTHER EVIDENCE FOR NON-MONOYNAPTIC GROUP-I EXCITATION OF MOTONEURONS IN THE HUMAN LOWER-LIMB, Experimental Brain Research, 115(1), 1997, pp. 35-46
Non-monosynaptic group I and group II excitation of human lower limb m
otoneurones was investigated. Changes in the firing probability of ind
ividual voluntarily activated motor units belonging to various muscles
(soleus, gastrocnemius medialis, tibialis anterior, peroneus brevis,
quadriceps and biceps femoris) were investigated after stimulation of
various nerves (posterior tibial, common peroneal and femoral nerves)
with weak (0.4-0.6xmotor threshold) electrical stimuli. In all investi
gated motor nuclei, stimulation of the ''homonymous'' nerve evoked a p
eak of increased firing probability with a latency that was 3-7 ms lon
ger than the monosynaptic Ia latency. The more caudal the motor nucleu
s explored, the greater the central delay. This strongly suggests a tr
ansmission through neurones located above the lumbar enlargement. If o
ne excepts the sural-induced excitation of peroneus brevis units, whic
h seems to be mediated through a particular pathway, the main peripher
al input to neurones mediating non-monosynaptic excitation evoked by t
hese weak stimuli is group I in origin. The pattern of distribution of
non-monosynaptic group I excitation was very diffuse, since stimulati
on of each nerve was able to evoke excitation in all investigated nucl
ei. In most cases, non-monosynaptic excitation evoked in a given motor
unit by stimulation of one nerve was depressed on combined stimulatio
n of two nerves, and evidence is presented that this lateral inhibitio
n is exerted at a premotoneuronal level. By contrast, there was no evi
dence that increasing the afferent input in a given pathway evokes an
''autogenetic'' inhibition in this pathway. The negative correlation f
ound between non-monosynaptic group I-induced and late group II-induce
d facilitation of the quadriceps H-reflex when using high stimulus int
ensities applied on the common peroneal nerve suggests that these two
effects could be mediated through common interneurones.