scholarly journals Autogenetic inhibition of extensor gamma-motoneurones revealed by electrical stimulation of group I fibres in the cat.

1983 ◽  
Vol 342 (1) ◽  
pp. 51-65 ◽  
Author(s):  
J Noth
1996 ◽  
Vol 75 (3) ◽  
pp. 1126-1137 ◽  
Author(s):  
G. W. Hiebert ◽  
P. J. Whelan ◽  
A. Prochazka ◽  
K. G. Pearson

1. In this investigation, we tested the hypothesis that muscle spindle afferents signaling the length of hind-leg flexor muscles are involved in terminating extensor activity and initiating flexion during walking. The hip flexor muscle iliopsoas (IP) and the ankle flexors tibialis anterior (TA) and extensor digitorum longus (EDL) were stretched or vibrated at various phases of the step cycle in spontaneously walking decerebrate cats. Changes in electromyogram amplitude, duration, and timing were then examined. The effects of electrically stimulating group I and II afferents in the nerves to TA and EDL also were examined. 2. Stretch of the individual flexor muscles (IP, TA, or EDL) during the stance phase reduced the duration of extensor activity and promoted the onset of flexor burst activity. The contralateral step cycle also was affected by the stretch, the duration of flexor activity being shortened and extensor activity occurring earlier. Therefore, stretch of the flexor muscles during the stance phase reset the locomotor rhythm to flexion ipsilaterally and extension contralaterally. 3. Results of electrically stimulating the afferents from the TA and EDL muscles suggested that different groups of afferents were responsible for the resetting of the step cycle. Stimulation of the TA nerve reset the locomotor step cycle when the stimulus intensity was in the group II range (2-5 xT). By contrast, stimulation of the EDL nerve generated strong resetting of the step cycle in the range of 1.2-1.4 xT, where primarily the group Ia afferents from the muscle spindles would be activated. 4. Vibration of IP or EDL during stance reduced the duration of the extensor activity by similar amounts to that produced by muscle stretch or by electrical stimulation of EDL at group Ia strengths. This suggests that the group Ia afferents from IP and EDL are capable of resetting the locomotor pattern generator. Vibration of TA did not affect the locomotor rhythm. 5. Stretch of IP or electrical stimulation of TA afferents (5 xT) during the flexion phase did not change the duration of the flexor activity. Stimulation of the EDL nerve at 1.8-5 xT during flexion increased the duration of the flexor activity. In none of our preparations did we observe resetting to extension when the flexor afferents were activated during flexion. 6. We conclude that as the flexor muscles lengthen during the stance phase of gait, their spindle afferents (group Ia afferents for EDL and IP, group II afferents for TA) act to inhibit the spinal center generating extensor activity thus facilitating the initiation of swing.


1995 ◽  
Vol 73 (3) ◽  
pp. 974-982 ◽  
Author(s):  
N. Kouchtir ◽  
J. F. Perrier ◽  
D. Zytnicki ◽  
L. Jami

1. Motoneurons innervating peroneal muscles were recorded intracellularly in anesthetized cats during sustained submaximal isometric contractions of peroneus brevis produced by repetitive electrical stimulation of motor axons in the distal portion of cut ventral root filaments. 2. In contrast with the inhibition previously observed during contractions of gastrocnemius medialis muscle in triceps surae motoneurons, the afferent input generated by peroneus brevis contraction elicited excitatory potentials in nearly all motoneurons supplying peroneus brevis, peroneus tertius, or peroneus longus muscles. 3. We ascribed the contraction-induced excitation of peroneal motoneurons to spindle afferents for two reasons. First, the amplitude of contraction-induced excitatory potentials increased when the ventral root stimulation strength was increased to recruit gamma-axons. Second, with stimulation strengths under gamma-threshold, peroneus brevis contraction still excited peroneal motoneurons, and we obtained evidence that activation of spindles by skeletofusimotor beta-axons could account at least partly for this excitation. 4. The lack of contraction-induced inhibition in peroneal motoneurons and the prevalence of contraction-induced excitation raised the possibility that, in contrast to the usual effects of tendon organ afferents, Ib afferents from peroneus brevis might exert an excitatory influence on homonymous motoneurons. The fact that electrical stimulation of group I afferents in the nerve to peroneus brevis only exceptionally evoked inhibition in peroneal motoneurons would appear compatible with this hypothesis. Furthermore, stimulation of cutaneous afferents, known to facilitate transmission in Ib pathways, only exceptionally revealed a weak contraction-induced inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)


1983 ◽  
Vol 49 (3) ◽  
pp. 649-661 ◽  
Author(s):  
K. D. Kniffki ◽  
K. Mizumura

1. The responses evoked by electrical stimulation of cutaneous and muscle nerves, by noxious and innocuous mechanical stimulation of muscle, tendon, and cutaneous tissues, and by intra-arterial (ia) injection of algesic substances (potassium, bradykinin) into arteries supplying the gastrocnemius-soleus muscle (GS) were studied in single neurons located in the ventroposterolateral nucleus (VPL) and in the transitional zone between VPL and the ventrolateral nucleus (VL) of cats lightly anesthetized with thiopenthal. Such chemical stimulation of the muscles has been shown to activate muscular groups III and IV axons specifically (43, 44) and presumably is nociceptive in character (14, 17, 31). 2. One hundred eight neurons were tested. Eighty-three of the units responded only to various types of cutaneous stimulation of the hindlimb. The other 25 responded to algesic stimulation of muscle and/or tendon. Of these latter 25, 7 had no apparent cutaneous receptive field although 4 of them responded to electrical stimulation of the common peroneal and/or sural nerve. Thus, only three neurons responded exclusively to algesic chemical and noxious mechanical stimulation of the muscle. Of the other 18 neurons, 14 had cutaneous receptive fields restricted to the hindlimb and often responded to non-noxious repetitive light stroking and to noxious pinching with a high-frequency discharge. Four cells (two of which had cutaneous input only from low-threshold mechanoreceptors) had complex and large receptive fields extending to more than one limb. 3. Potassium was a more potent muscle receptor stimulant than bradykinin, the latter only weakly exciting 3 neurons of 24 tested with both substances. The responses to potassium were rapid (approximately 4.0 s in latency) and tended to be greater (have higher response rates) for the units that responded to cutaneous as well as muscle/tendon stimulation. 4. Most neurons that responded to noxious deep stimulation had a threshold for the GS nerve volley in the group III fiber range. The few neurons with thresholds slightly below the group III range did not respond to activation of group I or II muscle spindle afferents by intra-arterial application of succinylcholine or by stretching the muscle. 5. Neurons with responses to any of the muscle, tendon, or cutaneous nociceptive stimuli were located at the ventral and dorsal periphery of VPL and in the VPL-VL transitional zone. 6. These results strongly suggest that there exist regions within the lateral diencephalon of cats that are capable of processing nociceptive information and that these regions are located at the periphery of VPL.


1985 ◽  
Vol 53 (2) ◽  
pp. 518-529 ◽  
Author(s):  
R. K. Powers ◽  
M. D. Binder

In the experiments described in the preceding paper electrical stimulation of the quadriceps (QUAD), medial tibial (MTIB), and flexor digitorum and hallucis longus (FDHL) muscle nerves was used to evoke oligosynaptic group I postsynaptic potentials (PSPs) in medial gastrocnemius (MG) motoneurons. In the present study, we attempted to specify the types of afferent fibers which mediate that oligosynaptic activity (FDHL to MG only). In one series of experiments, isolated single flexor digitorum longus (FDL) and flexor hallucis longus (FHL) afferents were identified as Ia, Ib, or group II fibers according to their conduction velocities, responses to muscle contraction, and mechanical thresholds to small amplitude triangular stretches applied to the parent muscles. We also determined the electrical thresholds of the identified afferent fibers by applying graded electrical stimulation to their muscle nerve. These results were used as criteria to define the types of afferents that mediated the electrically and stretch-evoked FDHL oligosynaptic PSPs recorded in MG motoneurons during a second series of experiments. The amplitudes of the oligosynaptic PSPs evoked in MG motoneurons increased as the strength of the electrical stimuli applied to the FDHL muscle nerves was raised to activate greater numbers of Ia- and Ib-fibers, but showed little or no additional increase when the stimulus intensity was raised further to include the majority of group II fibers. On this basis, a significant contribution by group II fibers to these oligosynaptic PSPs was considered unlikely. Simultaneous electrical activation of both Ia- and Ib-fibers produced distinct oligosynaptic PSPs in MG motoneurons, but these were likely due primarily to Ib-afferent activity, since selective activation of Ia-afferents (by stretch) rarely produced oligosynaptic PSPs in the same motoneurons. There was, however, evidence for some Ia contribution to these oligosynaptic PSPs. This is consistent with the demonstration that Ia- and Ib-afferent fibers converge onto common interneurons and that selective activation of Ia-fibers can produce PSPs similar to those evoked by concurrent stimulation of Ia- and Ib-fibers. On the basis of the present results and those of several related studies it is argued that the oligosynaptic PSPs evoked in MG motoneurons by submaximal group I stimulation of the FDHL, MTIB, or QUAD muscle nerves can be ascribed predominantly to the activation of Ib-afferent fibers, with only minimal Ia and probably no group II contribution.


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