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K G Pearson

Publications and source records attributed to K G Pearson.

At least 37 records · Page 2Linked to original sources
PubMed2000

Neural adaptation in the generation of rhythmic behavior.

Motor systems can adapt rapidly to changes in external conditions and to switching of internal goals. They can also adapt slowly in response to training, alterations in the mechanics of the system, and any changes in the system resulting from injury. This article reviews the mechanisms underlying short- and long-term adaptation in rhythmic motor systems. The neuronal networks underlying the generation of rhythmic motor patterns (central pattern generators; CPGs) are extremely flexible. Neuromodulators, central commands, and afferent signals all influence the pattern produced by a CPG by altering the cellular and synaptic properties of individual neurons and the coupling between different populations of neurons. This flexibility allows the generation of a variety of motor patterns appropriate for the mechanical requirements of different forms of a behavior. The matching of motor output to mechanical requirements depends on the capacity of pattern-generating networks to adapt to slow changes in body mechanics and persistent errors in performance. Afferent feedback from body and limb proprioceptors likely plays an important role in driving these long-term adaptive processes.

Adaptation, Physiological↗
PubMed2000

Stretch and H reflexes in triceps surae are similar during tonic and rhythmic contractions in high decerebrate cats.

During locomotion in decerebrate and spinal cats the group Ia afferents from hind leg muscles are depolarized rhythmically. An earlier study concluded that this locomotor-related primary afferent depolarization (PAD) does not contribute to modulation of monosynaptic reflex pathways during locomotion. This finding indicated that the neural network generating the locomotor rhythm, the central pattern generator (CPG), does not presynaptically inhibit monosynaptic reflexes. In this investigation we tested this prediction in decerebrate cats by measuring the magnitude of reflexes evoked in ankle extensor muscles during periods of tonic contractions and during sequences of rhythmic contractions. The latter occurred when the animal was induced to walk on a treadmill. At the similar levels of activity in the soleus muscle there was no significant difference in the magnitude of the soleus H reflex in these two behavioral situations. Similar results were obtained for reflexes evoked by brief stretches of the soleus muscle. We also examined the reflexes evoked by ramp-and-hold stretches during periods of rhythmic and tonic activity of the isolated medial gastrocnemius (MG) muscle. At similar levels of background activity, the reflexes evoked in the MG muscle were the same during rhythmic and tonic contractions. Our failure to observe a reduction in the magnitude of H reflexes and stretch reflexes during rhythmic contractions, compared with reflexes evoked at the same level of background activity during tonic contractions, is consistent with the notion that the CPG for stepping does not presynaptically inhibit monosynaptic reflexes during the extension phase of locomotor activity. Our results indicate that presynaptic inhibition of the monosynaptic reflex associated with normal locomotion in cats or humans arises from sources other than the extensor burst generating system of the central pattern generator.

Animals↗
PubMed1999

Contribution of sensory feedback to the generation of extensor activity during walking in the decerebrate Cat.

In this investigation we have estimated the afferent contribution to the generation of activity in the knee and ankle extensor muscles during walking in decerebrate cats by loading and unloading extensor muscles, and by unilateral deafferentation of a hind leg. The total contribution of afferent feedback to extensor burst generation was estimated by allowing one hind leg to step into a hole in the treadmill belt on which the animal was walking. In the absence of ground support the level of activity in knee and ankle extensor muscles was reduced to approximately 70% of normal. Activity in the ankle extensors could be restored during the "foot-in-hole" trials by selectively resisting extension at the ankle. Thus feedback from proprioceptors in the ankle extensor muscles probably makes a large contribution to burst generation in these muscles during weight-bearing steps. Similarly, feedback from proprioceptors in knee extensor appears to contribute substantially to the activation of knee extensor muscles because unloading and loading these muscles, by lifting and dropping the hindquarters, strongly reduced and increased, respectively, the level of activity in the knee extensors. This conclusion was supported by the finding that partial deafferentation of one hind leg by transection of the L4-L6 dorsal roots reduced the level of activity in the knee extensors by approximately 50%, but did not noticeably influence the activity in ankle extensor muscles. However, extending the deafferentation to include the L7-S2 dorsal roots decreased the ankle extensor activity. We conclude that afferent feedback contributes to more than one-half of the input to knee and ankle extensor motoneurons during the stance phase of walking in decerebrate cats. The continuous contribution of afferent feedback to the generation of extensor activity could function to automatically adjust the intensity of activity to meet external demands.

Afferent Pathways↗
PubMed1999

Adaptive changes in motor activity associated with functional recovery following muscle denervation in walking cats.

In this investigation we examined the changes in the pattern of activity in the medial gastrocnemius (MG) muscle in walking cats following transection of the nerves innervating synergist muscles (lateral gastrocnemius, soleus, and plantaris). Immediately following the nerve transections, there was a large increase in ankle flexion during early stance (from approximately 10 to approximately 30 degrees ) and a marked increase in the magnitude of the MG bursts during stance. We attribute this increase in the magnitude of the MG bursts to an increase in afferent feedback from the abnormally stretched MG muscle. During the week after the nerve transections, there was a progressive decrease in ankle yield. This improvement in ankle function was correlated with an increase in magnitude of two components of the MG bursts; the initial component starting during late swing and ending approximately 40 ms after ground contact, and a late component associated with stance. The time courses of the increases in the initial and late components of the MG bursts were different. Large and significant increases in the late component occurred the day after the nerve transections, whereas increases in the initial component occurred more gradually. This difference in time course was reflected in the kinematics of ankle movement. Over the first few days after the nerve transections, improvement in ankle movement occurred primarily late in the stance phase, and there was little change in ankle yield during early stance. At 1 wk, however, there was a significant reduction in ankle yield during early stance. This decreased yield was most likely due to an increase in stiffness of the MG muscle at the time of ground contact resulting from the increase in magnitude of the initial component of the MG bursts. The increases in the magnitude of the initial and late components of the MG bursts, as well as the improvement in ankle function, depended on use of the leg. All these changes were delayed by immobilizing the leg for 6 days in an extended position. We discuss possible mechanisms underlying the increase in the magnitude of the MG bursts and propose that proprioceptive signals from the stretched MG muscles provide an error signal for rescaling the magnitude of the centrally generated initial component. Our data support the concept that proprioceptive feedback functions to scale the magnitude of feed-forward motor commands to ensure they are appropriate for the biomechanical properties of the musculoskeletal system.

Adaptation, Physiological↗
PubMed1998

Enhancement and resetting of locomotor activity by muscle afferents.

The generation of the normal motor pattern for walking in mammals requires feedback from muscle proprioceptors. Two characteristics of the motor pattern particularly dependent on proprioceptive signals are (1) the magnitude of activity in knee and ankle extensor muscles and (2) the duration of extensor bursts during stance. Sensory regulation of these characteristics ensures that the level of activity in extensor muscles during stance is appropriate for the load carried by the leg and that the swing phase is not initiated when a leg is loaded. Many different groups of afferents from flexor and extensor muscles can influence the locomotor pattern. Most attention has focused on the action of group I afferents from ankle extensors. Electrical stimulation of these afferents during extension increases the duration and the magnitude of extensor activity. The prolongation of extensor activity depends in part on excitation of the extensor half-center by group Ib afferents from Golgi tendon organs. The enhancement of the magnitude of extensor bursts is produced primarily via disynaptic and polysynaptic pathways opened only during locomotion. The involvement of the proprioceptive signals in the generation of locomotor activity means that the gains in reflex pathways must be constantly calibrated according to the biomechanical properties of the locomotor system. Alteration of these properties by weakening ankle extensor muscles has recently been found to produce compensatory changes in proprioceptive influences on the locomotor pattern.

Animals↗
PubMed1997

Modification of group I field potentials in the intermediate nucleus of the cat spinal cord after chronic axotomy of an extensor nerve.

In walking decerebrate cats the influence of group I afferents from the medial gastrocnemius (MG) and the lateral gastrocnemius/soleus (LGS) muscles on stance phase duration is altered after axotomy of the LGS nerve [Whelan, P.J., Hiebert, G.W. and Pearson, K.G., J. Neurophysiol., 74 (1995) 2782-2787]. We examined whether a site for this plasticity is the connection from group I afferents onto spinal interneurons. Group I field potentials from MG, LGS and plantaris (PL) muscle afferents were recorded in the intermediate nucleus of the L6/L7 segments. Within 5 days following the transection of the LGS nerve in one hind leg, the field potential amplitudes from LGS afferents were decreased, from MG increased and those from PL were unchanged. The changes in the field potentials parallel modifications in the influence of group I afferents from the MG and LGS muscles on stance phase duration during walking.

Animals↗
PubMed1997

Effects of extensor muscle afferents on the timing of locomotor activity during walking in adult rats.

The influence of hind leg extensor muscle afferents on the timing of locomotor phase transitions was examined in adult, decerebrate rats, walking on a treadwheel. Walking occurred either spontaneously or was induced by stimulation of the mesencephalic locomotor region. Large diameter muscle afferents innervating the lateral or medial gastrocnemius were electrically stimulated during walking. A stimulus was delivered either at the onset of extensor muscle activity, or randomly during the step cycle. Stimulation with a train duration of 300 ms at the onset of extension increased the duration of the extensor bursts. The subsequent flexion phase was delayed. Stimulation with a shorter stimulus train (150 ms) early in extension had little effect on the extension phase duration. However when delivered at the end of extension the same stimulus significantly increased the duration of the extension phase and decreased the duration of the following flexion phase. Stimulating near the end of the flexion phase delayed onset and decreased duration of the subsequent extension phase. The effects of stimulating extensor afferents during the extension phase were weaker but qualitatively similar, to those in cats, suggesting similar mechanisms. The results of this study also show major differences in the integration of extensor muscle afferents between adult and neonatal rats.

Afferent Pathways↗
PubMed1997

Comparison of the effects of stimulating extensor group I afferents on cycle period during walking in conscious and decerebrate cats.

Previous studies have reported that stimulation of group I afferents from extensor muscles prolongs stance duration during walking in decerebrate cats. The main objective of this investigation was to determine whether this phenomenon occurs during walking in conscious cats. In conscious cats without lesions of the central nervous system (CNS), stimulation of group I afferents in the lateral gastrocnemius/soleus (LGS) nerve during stance prolonged extensor burst duration and increased the cycle period in five of seven animals. The mean increases in cycle period were modest, ranging from 6 to 22%. In five of six animals that walked both quadrupedally and bipedally at the same rate, the effects on cycle period were stronger during bipedal stepping (18% mean increase in cycle period compared with 9%). The stimulated nerves were transected and the experimental procedure was usually delayed in the conscious animals for 2-3 days following implantation of the stimulating electrodes. To assess whether chronic axotomy of the LGS nerve was a factor in the decreased effectiveness, four of the cats with chronic nerve section were decerebrated and their LGS nerves were stimulated after the animals began to spontaneously walk on a motorized treadmill. In all four of these animals, the effects of stimulating the chronically cut LGS nerve on the step cycle period became stronger following decerebration. However, these effects were not as strong as those produced when an acutely sectioned LGS nerve was stimulated. During both quadrupedal and bipedal walking, stimulation of the LGS nerve increased the amplitude of the medial gastrocnemius (MG) electromyogram. The augmented activity of the MG muscle contributed to an increased extension of the ankle during stimulated steps. The conclusion from these experiments is that stimulation of the group I afferents in extensor nerves can prolong stance in the conscious cat, but this effect is weaker than in decerebrate animals. It is likely that transmission in the polysynaptic group I pathways controlling stance duration is regulated in a complex fashion by descending signals from the brain in the conscious animal.

Afferent Pathways↗
PubMed1997

Plasticity in reflex pathways controlling stepping in the cat.

Previous studies have shown that stimulation of group 'I' afferents from ankle extensor muscles can prolong the cycle period in decerebrate walking cats and that the magnitude of these effects can be altered after chronic axotomy of the lateral-gastrocnemius/soleus (LGS) nerve. The effectiveness of LGS group I afferents in prolonging the cycle period decreases after axotomy, whereas the effectiveness of the uncut medial-gastrocnemius (MG) group I afferents is increased. The objectives of this investigation were to establish the time course of these changes in effectiveness and to determine whether these changes persist after transection of the spinal cord. The effects of stimulating the LGS and/or MG group I afferents on the cycle period were examined in 22 walking decerebrate animals in which one LGS nerve had been cut for 2 to 31 days. The effectiveness of LGS group I afferents declined progressively in the postaxotomy period, beginning with significant decreases at 3 days and ending close to zero effectiveness at 31 days. Large increases in the effectiveness of MG group I afferents occurred 5 days after axotomy, but there was no progressive change from 5 to 31 days. To test whether these changes in effectiveness were localized to sites within the spinal cord, the cord was transected in some decerebrate animals and stepping induced by the administration of L-DOPA L-3-4 dihydroxyphenylalanine (L-DOPA) and Nialamide. The effects of stimulating the MG and/or the LGS group I afferents on the cycle period were reexamined. In all four animals tested, stimulating the axotomized LGS group I afferents had a reduced effectiveness during locomotor activity in both the decerebrate and spinal states, whereas the increased effectiveness of the MG group I afferents was retained after transection of the spinal cord in two of five animals. Different mechanisms may be responsible for the changes in strength of the LGS and MG group I afferent pathways that project onto the rhythm generating sites in the spinal cord. This possibility follows from our observations of a linear relationship between the time after axotomy and decreased effectiveness of LGS group I afferents but no significant relationship between time postaxotomy and increased effectiveness of MG group I afferents; no significant relationship between the decreased effectiveness of LGS group I afferents and the increased effectiveness of MG group I afferents; and, after spinalization, consistent (4/4 cases) preservation of decreased LGS effectiveness but frequent (3/5 cases) loss of increased MG effectiveness.

Animals↗
PubMed1997

Stretch of quadriceps inhibits the soleus H reflex during locomotion in decerebrate cats.

Previously, it has been demonstrated that afferent signals from the quadriceps muscles can suppress H reflexes in humans during passive movements of the leg. To establish whether afferent input from quadriceps contributes to the modulation of the soleus H reflex during locomotion, the soleus H reflex was conditioned with stretches of the quadriceps muscle during bouts of spontaneous treadmill locomotion in decerebrate cats. We hypothesized that 1) in the absence of locomotion such conditioning would lead to suppression of the soleus H reflex and 2) this would be retained during periods of locomotor activity. In the absence of locomotion, slow sinusoidal stretches (0.2 Hz, 8 mm) of quadriceps cyclically modulated the amplitude of the soleus H reflex. The H reflex amplitude was least during the lengthening of the quadriceps and greatest as quadriceps shortened. Further, low-amplitude vibrations (48-78 micron) applied to the patellar tendon suppressed the reflex, indicating that the muscle spindle primaries were the receptor eliciting the effect. During bouts of locomotion, ramp stretches of quadriceps were applied during the extensor phase of the locomotor rhythm. Soleus H reflexes sampled at two points during the stance phase were reduced compared with phase-matched controls. The background level of the soleus electromyographic activity was not influenced by the applied stretches to quadriceps, either during locomotion or in the absence of locomotion. This indicates that the excitability of the soleus motoneuron pool was not influenced by the stretching of quadriceps, and that the inhibition of the soleus H reflex is due to presynaptic inhibition. We conclude that group Ia afferent feedback from quadriceps contributes to the regulation of the soleus H reflex during the stance phase of locomotion in decerebrate cats. This afferent mediated source of regulation of the H reflex, or monosynaptic stretch reflex, would allow for rapid alterations in reflex gain according to the dynamic needs of the animal. During early stance, this source of regulation might suppress the soleus stretch reflex to allow adequate yielding at the ankle and facilitate the movement of the body over the foot.

Animals↗
PubMed1996

Contribution of hind limb flexor muscle afferents to the timing of phase transitions in the cat step cycle.

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.

Afferent Pathways↗
PubMed1995

Disynaptic group I excitation of synergist ankle extensor motoneurones during fictive locomotion in the cat.

1. Intracellular recording from medial gastrocnemius (MG) motoneurones was used to examine postsynaptic potentials produced by electrical stimulation of the plantaris nerve at group I strength at rest and during fictive locomotion. Fictive locomotion was evoked by stimulation of the midbrain locomotor region (MLR) in decerebrate cats or in decerebrate, acute low-spinal cats by perineal stimulation following intravenous administration of clonidine and naloxone. 2. In both MLR and spinal fictive locomotor preparations, stimulation of plantaris nerve group I afferents at rest evoked short-latency (< 2 ms) IPSPs in MG motoneurones. During the extensor phase of MLR-evoked locomotion, the same stimulation produced short-latency (1.6-1.8 ms) EPSPs. Such latencies suggest mediation by one interneurone interposed between plantaris nerve group I afferents and MG motoneurones. Non-monosynaptic, short-latency excitation was not seen at rest nor during the flexion phase of the step cycle. 3. Group I EPSPs during the extensor phase of MLR-evoked locomotion were evoked by stimulation at intensities ranging from 1.4-2 times threshold (T). The effectiveness of stimulation intensities < 1.5 T suggests that activation of group II afferents is not required to evoke disynaptic excitation. Selective activation of group Ia afferents by stretches of the Achilles tendon also produced disynaptic EPSPs during extension. 4. During fictive locomotion in spinal animals pretreated with clonidine, short-latency group I EPSPs were not seen but group I IPSPs recorded at rest disappeared or were greatly attenuated. The failure of depolarizing current to reveal group I IPSPs suggests that fictive locomotion involves an inhibition of the inhibitory interneurones that operate at rest. In both clonidine-treated spinal and MLR preparations, trains of stimuli at group I strength evoked longer-latency and slowly rising potentials that were more prominent during the flexor phase of fictive locomotion. 5. These results show a reduction in short-latency group I inhibition of synergists in both MLR and clonidine-treated spinal preparations during fictive locomotion. In addition, activation of group I afferents evokes short-latency excitation of synergists during extension in the MLR preparation. Such excitatory reflexes activated by ankle extensor group Ia and Ib afferents may form an excitatory feedback system, reinforcing on-going extensor activity during the stance phase of the step cycle.

Animals↗
PubMed1995

Stimulation of the group I extensor afferents prolongs the stance phase in walking cats.

Group I afferents in nerves innervating the lateral gastrocnemius-soleus (LG-Sol), plantaris (Pl), and vastus lateralis/intermedius (VL/VI) muscles were stimulated during walking in decerebrate cats. The stimulus trains were triggered at a fixed delay following the onset of bursts in the medial gastrocnemius muscle. Stimulation of all three nerves with long stimulus trains (> 600 ms) prolonged the extensor bursts and delayed the onset of flexor burst activity. LG-Sol nerve stimulation had the strongest effect; often delaying the onset of flex- or burst activity until the stimulus train was ended. By contrast, flexor bursts were usually initiated before the end of the stimulus train to the Pl and VL/VI nerves. The minimum stimulus strength required to increase the cycle period was between 1.3 x threshold and 1.6 x threshold for all three nerves. Simultaneous stimulation of the Pl and VL/VI nerves produced a larger effect on the cycle period than stimulation of either nerve alone. The spatial summation of inputs from knee and ankle muscles suggests that the excitatory action of the group I afferents during the stance phase is distributed to all leg extensor muscles. Stimulation of the group I afferents in extensor nerves generally produced an increase in the amplitude of the heteronymous extensor EMG towards the end of the stance phase. This increase in amplitude occurred even though there were only weak monosynaptic connections between the stimulated afferents and the motoneurones that innervated these heteronymous muscles. This suggests that the excitation was produced via oligosynaptic projections onto the extensor motoneuronal pool. Stimulation with 300 ms trains during the early part of flexion resulted in abrupt termination of the swing phase and reinitiation of the stance phase of the step cycle. The swing phase resumed coincidently with the stimulus offset. Usually, stimulation of two extensor nerves at group I strengths was required to elicit this effect. We were unable to establish the relative contributions of input from the group Ia and group Ib afferents to prolonging the stance phase. However, we consider it likely that group Ib afferents contribute significantly, since their activation has been shown to prolong extensor burst activity in reduced spinal preparations. Thus, our results add support to the hypothesis that unloading of the hindlimb during late stance is a necessary condition for the initiation of the swing phase in walking animals.

Action Potentials↗
PubMed1995

Proprioceptive regulation of locomotion.

Recent investigations of proprioreceptors in the walking systems of cats, insects and crustaceans have identified reflex pathways that regulate the timing of the transition from stance to swing, and control the magnitude of ongoing motoneuronal activity. An important finding in the cat is that during locomotor activity, the influence of feedback from the Golgi tendon organs in extensor muscles onto extensor motoneurons is reversed from inhibition to excitation. The excitatory action of tendon organs during stance ensures that stance is maintained while extensor muscles are loaded, and may regulate the magnitude of extensor activity according to the load carried by the leg. Afferents from primary and secondary spindles in extensor and flexor muscles have also been found to influence the timing of the locomotor rhythm in a functionally relevant manner. Recent studies indicate that reflex reversals and the regulation of timing by multiple proprioceptive systems are also features of walking systems in arthropods.

Animals↗
PubMed1995

Suppression of the corrective response to loss of ground support by stimulation of extensor group I afferents.

1. When a hind leg of a walking cat fails to contact the ground at the end of swing, the limb is rapidly lifted and replaced in an attempt to seek support. In this investigation we tested the hypothesis that one factor in the initiation of this corrective response is the absence of signals from the group I afferents of extensor muscles. 2. Experiments were performed on decerebrate cats walking on a treadmill. The corrective response to loss of ground support occurred when one hind leg stepped into a hole cut into the treadmill belt. Group I afferents in various extensor nerves were stimulated via implanted cuff electrodes when the foot entered the hole. 3. Stimulation of extensor group I afferents suppressed the corrective flexion response. Instead of a flexor burst being generated soon after the foot entered the hole, extensor activity was maintained for a period exceeding the duration of the stimulus trains. The onset of the corrective response occurred at a relatively fixed latency of 70 ms after the end of the short stimulus trains (200-400 ms) provided that the contralateral limb was still in stance phase. For longer stimulus trains (500-1,000 ms) that terminated during or just prior to the swing phase of the contralateral leg, the onset of ipsilateral flexor activity occurred only after the contralateral leg had regained support. 4. We conclude that the absence of signals from group I afferents when a foot fails to contact the ground allows the locomotor rhythm generator to re-initiate a flexor burst to produce the corrective response.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1995

Plasticity of the extensor group I pathway controlling the stance to swing transition in the cat.

1. This study examines whether the efficacy of polysynaptic group I excitatory pathways to extensor motoneurons are modified after axotomy of a synergistic nerve. Previously, it has been shown that stimulation of extensor nerves at group I strength can extend the stance phase and delay swing. Stimulation of the lateral gastrocnemius and soleus (LG/S) nerve prolongs stance for the duration of the stimulus train, whereas stimulation of the medial gastrocnemius (MG) nerve moderately increases stance. Our hypothesis was that after axotomy of the LG/S nerve the efficacy of the MG group I input would increase. 2. This idea was tested in 10 adult cats that had their left LG/S nerves axotomized for 3-28 days. On the experimental day the cats were decerebrated and the left (experimental) and right (control) LG/S and MG nerves were stimulated during late stance as the animals were walking on a motorized treadmill. A significant increase in the efficacy of the left MG nerve occurred 5 days after axotomy of the LG/S nerve when compared with the control response. By contrast, the previously cut LG/S nerve showed a reduction in efficacy after 3 days compared with the control limb. 3. Functionally, this plasticity may be an important mechanism by which the strength of the group I pathway is calibrated to different loads on the extensor muscles.

Animals↗
PubMed1994

Corrective responses to loss of ground support during walking. II. Comparison of intact and chronic spinal cats.

1. The preceding study described a corrective response in cats when one hind leg steps into a hole. In this investigation we examine the extent to which this behavior is organized at the spinal level by comparing the responses elicited in intact and chronic spinal cats. 2. Adult cats were trained to step bipedally with their hind legs on a treadmill. After training, the responses to stepping into a hole cut in the treadmill belt were monitored with a video recorder and by recording electromyograms from muscles in both hind legs. The responses to stepping into the hole were also recorded in chronic spinal cats that had recovered the ability to step with their hind legs a few weeks after spinalization. 3. The behavioral responses in the two groups of animals differed in two respects. First, the latency of the onset of the flexion movement to remove the foot from the hole was shorter in intact animals (70-150 ms in intact vs. 130-350 ms in spinal animals). Second, the flexion movement in the intact animals was stronger. The exaggerated flexion movement in intact animals lifted the paw well clear of the hole and allowed support to be regained on the treadmill belt. The weaker flexion movement in spinal animals was usually insufficient to lift the paw completely from the hole. 4. Differences in the motor patterns recorded from flexor muscles during the corrective response in intact and spinal animals correspond with the differences in the kinematics. First, the onset of flexor activity after the foot entered the hole was delayed by approximately 100 ms in spinal animals relative to intact animals. Second, in intact animals the magnitudes of flexor bursts were increased relative to the flexor bursts associated with the swing phase during stepping, whereas in spinal animals flexor bursts during the corrective response resembled those occurring during swing. 5. Similarities in the duration and the timing of bursts in different flexor muscles in intact and spinal animals during the corrective response and during swing indicated that the corrective response involves activation of the spinal system that normally produces swing phase flexor activity. We conclude that activation of this system is facilitated by input from supraspinal structures during the corrective response in intact animals. 6. In all intact animals and three of five spinal animals, support of the hindquarters when the foot entered the hole was maintained by the contralateral leg.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗