How is load sensed by receptors, and how is this sensory information used to guide locomotion? Many insights in this domain have evolved from comparative studies since it has been realized that basic principles concerning load sensing and regulation can be found in a wide variety of animals, both vertebrate and invertebrate. Feedback about load is not only derived from specific load receptors but also from other types of receptors that previously were thought to have other functions. In the central nervous system of many species, a convergence is found between specific and nonspecific load receptors. Furthermore, feedback from load receptors onto central circuits involved in the generation of rhythmic locomotor output is commonly found. During the stance phase, afferent activity from various load detectors can activate the extensor part in such circuits, thereby providing reinforcing force feedback. At the same time, the flexion is suppressed. The functional role of this arrangement is that activity in antigravity muscles is promoted while the onset of the next flexion is delayed as long as the limb is loaded. This type of reinforcing force feedback is present during gait but absent in the immoble resting animal.

1. Stimulation of different hindlimb nerves in spontaneously walking premammillary cats was used in order to examine the effects of sensory input on the rhythmic motor output. 2. Stimulation of the tibial or sural nerve at low intensities caused the burst of activity in the triceps surae or semimembranosus to be prolonged if stimuli were given during the extension phase. When applied during the flexion phase, the same stimuli shortened the burst of activity in the pretibial flexors and induced an early onset of the extensor activity, except if stimuli were given at the very beginning of the flexion phase, when flexor burst prolongations or rebounds were observed instead. 3. These effects were related to activation of large cutaneous afferents in these nerves since the results could be duplicated by low-intensity stimulation of the tibial nerve at the ankle or by direct stimulation of the pad. 4. In contrast, activation of smaller afferents by high-intensity stimulation resulted prolongations of the flexor burst and/or shortenings of the extensor burst for stimuli applied before or during these bursts, respectively. 5. It was concluded that the large and small cutaneous afferents make, respectively, inhibitory and excitatory connections with the central structure involved in the generation of flexion during walking.

Please be advised that this information was generated on 2018-05-12 and may be subject to change.Journal o r N eu ro ph y sio lo g y Vol. 76, No. I. July 1996. Printed in U.S.A. 1 . The phase-dependent modulation of medium-latency (P2) (70-80 ms) responses in semitendinosus (ST), biceps femoris (BF), rectus femoris (RF), and tibialis anterior (TA) was studied with the use of low-intensity stimulation (2 times perception threshold) of the sural nerve. The shocks were given in a random order at 16 phases of the step cycle in 10 normal subjects during forward walking (FW) or backward walking (BW) on a treadmill. Backward and Forward Walking Use Different Patterns of PhaseDependent Modulation of Cutaneous Reflexes in Humans2. All subjects exhibited P2 responses in all muscles studied both during BW and FW. The amplitude of the facilitatory P2 responses showed phase-dependent changes that could not have been predicted on the basis of the variations in background activity throughout the step cycle.5. During FW, the P2 facilitatory responses in BF were large (with respect to the background activity) throughout the whole step cycle except for a short period near the end of the swing phase. In ST the responses were smaller and appeared primarily at the end of the stance phase and during the first part of the swing phase. During the second half of swing the P2 responses were basically suppressive. A modulation pattern similar to the one in ST was found in RF and TA, except that there was no reversal to suppressive responses in the swing phase in RF. Instead, a reduc tion in the amplitude of the facilitatory P2 responses occurred.4. During BW, the modulation pattern recorded in the same subjects was different from the one seen during FW. Large facilita tory P2 responses were present in all muscles in middle and late swing. In the first half of stance the responses were most promi nently seen in BF and RF. At the end of stance and/or at the onset of swing the facilitatory responses decreased in amplitude (BF and RF) or reversed to P2 suppressions (ST and TA).5. We conclude that there are both facilitatory and suppressive pathways from the sural nerve to the leg muscles studied and that the balance of activity in these paths is phase dependent during both FW and BW. It is suggested that the phase-dependent modula tion of P2 responses could largely rely on a central motor program. During BW the same motor program is used as during FW, but possibly running in reverse, thereby causing a shift both in the timing of the reflex reversal and in the periods of reflex suppression.

1. The modulation of reflex responses in up to 10 simultaneously recorded hindlimb muscles was studied in unrestrained cats walking on a treadmill. Single electrical shocks of various strengths were applied to different skin areas of teh hindlimb at different times of the step cycle while the resulting EMG responses were sampled and analyzed. 2. Two excitatory response peaks (P1 and P2) at a latency of about 10 and 25 ms, respectively, were seen in all flexors examined (sartorius, semitendinosus, tibialis anterior, extensor digitorum longus). Stimulation of most skin areas was effective but responses were most easily obtained from stimuli applied to the foot or ankle. During the step cycle there was a marked modulation of the amplitudes of the responses, especially the P2 responses, which grew larger toward the end of stance when a maximum was reached, followed by a steady decline throughout swing. This pattern was very similar for various flexors, although these muscles differed considerably in their normal EMG activity pattern during walking. 3. Flexor responses were absent when the same stimuli were applied during the early stance phase. Instead, inhibition of the ongoing EMG activity was seen at a latency of 10 ms or less in all extensors examined (semimembranosus, quadriceps, soleus, gastrocnemius medialis, flexor digitorum longus). The inhibition was followed by a late excitatory peak (P3) at about 35-ms latency in all extensors except soleus. 4. Certain stimulation sites yielded exceptions to the above patterns. Stimulation of the skin area innervated by the sural nerve yielded larger and earlier MG excitatory responses as compared to stimulation of other skin areas. Activation of the plantar surface of the foot often failed to elicit P2 responses in the hip flexor sartorius, which showed inhibition instead. 5. In the hindlimb contralateral to the stimulus, excitatory responses occurred both in flexors and extensors at a latency of 20-25 ms. The pattern of modulation of these responses was similar to the ipsilateral modulation of P2 flexor and P3 extensor responses. Soleus failed to show a crossed response. 6. The data indicate that flexor and extensor responses differ both with respect to their latency and to their correlation with the ongoing EMG reactivity. It is concluded that these stimuli do not demonstrate reflex reversal in the strict sense in the normal walking cat but that there is modulation of transmission in a flexor excitatory and extensor inhibitory pathway, possibly by the flexor part of the spinal locomotor oscillator. In addition, there are some specialized flexor inhibitory and extensor excitatory pathways. The slow soleus muscle does not seem to be excited through these pathways.

No abstract