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At least 73 records · Page 4Linked to original sources

PubMed2006

Modulation of respiratory activity by locomotion in lampreys.

In vertebrates, locomotion is associated with changes in respiratory activity, but the neural mechanisms by which this occurs remain unknown. We began examining this in lampreys using a semi-intact preparation of young adult Petromyzon marinus, in which respiratory and locomotor behaviors can be recorded simultaneously with the activity of the underlying neural control systems. Spontaneous fictive respiration was recorded with suction electrodes positioned over the glossopharyngeal or the rostral vagal motor nucleus. In this preparation, locomotor activity, characterized by symmetrical tail movements (electromyogram recordings), was evoked by mechanical stimulation of the skin. During locomotion, the mean respiratory frequency and the mean area of the motor bursts were significantly increased (81.6+/-28.6% and 62.8+/-25.4%, respectively; P<0.05). The frequency returned to normal 92+/-51 s after the end of locomotion. There were fluctuations in the instantaneous respiratory and locomotor frequencies that were rhythmical but antiphasic for the two rhythmic activities. The changes in respiratory activity were also examined during bouts of locomotion occurring spontaneously, and it was found that a modification in respiratory activity preceded the onset of spontaneous locomotion by 3.5+/-2.6 s. This suggests that the early respiratory changes are anticipatory and are not caused by feedback generated by locomotion. The increase in respiratory frequency during locomotion induced by sensory stimulation persisted after removal of the mesencephalon. When both the mesencephalon and spinal cord were removed, resulting in the isolation of the rhombencephalon, changes in the respiratory activity were also present following skin stimulations that would have normally induced locomotion. Altogether, the results suggest that respiratory changes are programmed to adjust ventilation prior to motor activity, and that a central rhombencephalic mechanism is involved.

Action Potentials↗

PubMed1981

Energy cost and cardiopulmonary responses for wheelchair locomotion and walking on tile and on carpet.

The purpose of this study was to compare energy cost and cardiopulmonary responses to wheelchair locomotion and walking on tile and on carpet at 3.0 km . h-1. Nine wheelchair-dependent (WD) and ten able-bodied (AB) individuals served as test subjects. WD subjects were tested for wheelchair locomotion on tile and on carpet, and AB subjects were tested for walking over both floor surfaces. Studied variables included gross energy cost (GEC), net locomotive energy cost (NLEC), pulmonary ventilation (VE) and heart rate (HR) during all test conditions. On tile, GEC and NLEC were found to be lower, whereas VE and HR were higher for wheelchair locomotion than for walking. On carpet, wheelchair locomotion elicited higher values for all variables than walking. In going from tile to carpet, significant increases in these variables were found for wheelchair locomotion, whereas walking elicited similar response magnitudes on both floor surfaces. These results suggest that cardiopulmonary stresses for wheelchair locomotion are higher than for walking, and that a carpet can present an obstacle to wheelchair locomotion which may not be recognised by those who walk.

Adult↗

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↗

PubMed2000

Does autonomic blockade reveal a potent contribution of nitric oxide to locomotion-induced vasodilation?

We sought to test the role of nitric oxide (NO) in governing skeletal muscle (iliac) vascular conductance during treadmill locomotion in dogs (n = 6; 3.2 and 6.4 km/h at 0% grade, and 6.4 km/h at 10% grade). As seen previously, the increase in muscle vascular conductance accompanying treadmill locomotion was little influenced by NO synthase inhibition alone with N(omega)-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv), but the absolute value of conductance achieved during locomotion was reduced. Such ambiguous results provide an unclear picture regarding the importance of NO during locomotion. However, muscle vasodilation is normally restrained by the sympathetic system during locomotion. Thus a significant contribution by NO to the increase in vascular conductance that accompanies locomotion could be masked by partial withdrawal of the competing influence of sympathetic vasoconstrictor nerve activity secondary to the rise in arterial pressure following systemic L-NAME administration. To test this possibility, we compared the rise in muscle vascular conductance before and after L-NAME treatment while ganglionic transmission was blocked by hexamethonium. Under these conditions, L-NAME significantly reduced both the rise in vascular conductance (by 32%, P < 0.001) and the absolute level of vascular conductance (by 30%, P < 0.001) achieved during locomotion with no effect on blood flow. Thus augmented NO production normally provides a significant drive to relax vascular smooth muscle in active skeletal muscle during locomotion. Potential deficits stemming from the absence of NO following L-NAME treatment are masked by less intense sympathetic restraint when autonomic function is intact.

Animals↗

PubMed1993

Stimulation of vagal afferents inhibits locomotion in mesencephalic cats.

Using electrical stimulation of the mesencephalic locomotor region, we made decerebrate unanesthetized cats walk on a treadmill. The locomotion induced by stimulation of this midbrain area was assessed before and during activation of vagal afferents by either intravenous injection of phenylbiguanide or inflation of a balloon placed in the left atrium. Inflation of a balloon, which increased left atrial pressure by 7-25 mmHg, abolished locomotion in 9 of 10 cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by balloon inflation in each of two cats tested. Intravenous phenylbiguanide (50 or 100 micrograms/kg) or serotonin (40 micrograms/kg) injections abolished or attenuated walking induced by midbrain stimulation in 11 of 13 cats tested. In addition, intravenous phenylbiguanide injections abolished or attenuated locomotion with a shorter onset time than did systemic injections of this substance in five of six cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by phenylbiguanide injection in each of five cats tested. We conclude that locomotion can be prevented by a viscerosomatic reflex arising from the lungs and heart. The afferent arm of this reflex arc is the vagus nerve. Afferents such as slowly and rapidly adapting pulmonary stretch receptors, atrial receptors, and lung C-fibers may have had a role in preventing locomotion during the increase in left atrial pressure in our experiments. On the other hand, pulmonary C-fibers had a crucial role in preventing locomotion during intravenous injection of phenyl-biguanide. We speculate that this viscerosomatic reflex may help to explain in part the intolerance for exercise displayed by patients with congestive heart failure.

Animals↗

PubMed2001

Twisting and bending: the functional role of salamander lateral hypaxial musculature during locomotion.

The function of the lateral hypaxial muscles during locomotion in tetrapods is controversial. Currently, there are two hypotheses of lateral hypaxial muscle function. The first, supported by electromyographic (EMG) data from a lizard (Iguana iguana) and a salamander (Dicamptodon ensatus), suggests that hypaxial muscles function to bend the body during swimming and to resist long-axis torsion during walking. The second, supported by EMG data from lizards during relatively high-speed locomotion, suggests that these muscles function primarily to bend the body during locomotion, not to resist torsional forces. To determine whether the results from D. ensatus hold for another salamander, we recorded lateral hypaxial muscle EMGs synchronized with body and limb kinematics in the tiger salamander Ambystoma tigrinum. In agreement with results from aquatic locomotion in D. ensatus, all four layers of lateral hypaxial musculature were found to show synchronous EMG activity during swimming in A. tigrinum. Our findings for terrestrial locomotion also agree with previous results from D. ensatus and support the torsion resistance hypothesis for terrestrial locomotion. We observed asynchronous EMG bursts of relatively high intensity in the lateral and medial pairs of hypaxial muscles during walking in tiger salamanders (we call these 'alpha-bursts'). We infer from this pattern that the more lateral two layers of oblique hypaxial musculature, Mm. obliquus externus superficialis (OES) and obliquus externus profundus (OEP), are active on the side towards which the trunk is bending, while the more medial two layers, Mm. obliquus internus (OI) and transversus abdominis (TA), are active on the opposite side. This result is consistent with the hypothesis proposed for D. ensatus that the OES and OEP generate torsional moments to counteract ground reaction forces generated by forelimb support, while the OI and TA generate torsional moments to counteract ground reaction forces from hindlimb support. However, unlike the EMG pattern reported for D. ensatus, a second, lower-intensity burst of EMG activity ('beta-burst') was sometimes recorded from the lateral hypaxial muscles in A. tigrinum. As seen in other muscle systems, these beta-bursts of hypaxial muscle coactivation may function to provide fine motor control during locomotion. The presence of asynchronous, relatively high-intensity alpha-bursts indicates that the lateral hypaxial muscles generate torsional moments during terrestrial locomotion, but it is possible that the balance of forces from both alpha- and beta-bursts may allow the lateral hypaxial muscles to contribute to lateral bending of the body as well.

Ambystoma↗

PubMed2003

Activity of different classes of neurons of the motor cortex during locomotion.

This study examines the activity of different classes of neurons of the motor cortex in the rabbit during two locomotion tasks: a simple (on a flat surface) and a complex (overstepping a series of barriers) locomotion. Four classes of efferent neurons were studied: corticocortical (CC) neurons with ipsilateral projection (CCIs), those with contralateral projection (CCCs), descending corticofugal neurons of layer V (CF5s), and those of layer VI (CF6s). In addition, one class of inhibitory interneurons (SINs) was investigated. CF5 neurons and SINs were the only groups that were strongly active during locomotion. In most of these neurons a clear-cut modulation of discharge in the locomotion rhythm was observed. During simple locomotion, CF5s and SINs were preferentially active in opposite phases of the step cycle, suggesting that SINs contribute to formation of the step-related pattern of CF5s. Transition from simple to complex locomotion was associated with changes of the discharge pattern of the majority of CF5 neurons and SINs. In contrast to CF5 neurons, other classes of efferent neurons (CCI, CCC, CF6) were much less active during both simple and complex locomotion. That suggests that CC interactions, both within a hemisphere (mediated by CCIs) and between hemispheres (mediated by CCCs), as well as corticothalamic interactions via CF6 neurons are not essential for motor coordination during either simple or complex locomotion tasks.

Action Potentials↗

PubMed2000

Protein kinase C isoforms involved in regulation of cell shape and locomotion of human fibrosarcoma HT1080 cells.

The role of protein kinase C (PKC) isoforms in the regulation of cell shape [switch between fibroblast-like and crescent shape (CS)] and of locomotion of human fibrosarcoma HT1080 cells has been investigated. The PKC activator phorbol myristate acetate (PMA) induced the transition of elongated fibroblast-like cells into CS cells and stimulated locomotion. Both responses to PMA were inhibited by the PKC inhibitor Ro 31-8220. Analysis of the time course showed that stimulation of shape changes (formation of CS cells) and locomotor activity (increase in the proportion and speed of locomoting cells) was maximal in the early phase of the response (up to 2.5 hr) and significantly decreased later (15 to 21 hr). CS formation and stimulated locomotion correlated closely with a marked redistribution from the cytosol to the membrane of PKC isoforms alpha, beta1 and gamma in the early phase (0.5 to 2 hr) following activation with PMA. The subsequent reduction of the proportion of CS cells and of cell locomotion correlated with down-regulation of these isoforms in the second phase (16 to 21 hr). In contrast, the total amount and distribution of PKC beta2 remained almost unchanged with 10(-8) M PMA up to 21 hr. Furthermore, changes in shape and locomotion did not correlate with the responses of PKC delta to PMA. Inhibition of PMA-stimulated locomotion by the more specific inhibitor Gö 6976 is consistent with a role of PKC alpha and beta1 in this response. Ro 31-8220 alone induced a moderate down-regulation of PKC isoforms alpha and delta, but it also inhibited the more pronounced down-regulation of these isoforms by PMA. Our results indicate that activation of PKC isoforms alpha, gamma and beta1, but not beta2 or delta, stimulates locomotion and formation of CS cells in human fibrosarcoma HT1080 cells.

Carbazoles↗

PubMed1994

Selective effects of the PKC inhibitors Ro 31-8220 and CGP 41,251 on PMN locomotion, cell polarity, and pinocytosis.

Using two newly synthesized inhibitors, Ro 31-8220 and CGP 41,251, of protein kinase C (PKC), we analysed: (1) how distinct PMN functions (shape changes, locomotion, pinocytosis) are regulated, and (2) the role of protein phosphorylation and PKC in this process. We were able to transform: (1) resting PMNs into locomoting cells using fNLPNTL, (2) locomoting cells into non-locomoting highly pinocytic cells using PMA, and (3) PMA-stimulated cells showing marked pinocytosis into locomoting or into resting cells using Ro 31-8220. It is thus possible to selectively manipulate PMN function (resting state, locomotion, marked pinocytosis), indicating that there are different regulatory pathways. It was not possible to induce locomotion and marked pinocytosis simultaneously, indicating crosstalk between pathways. Ro 31-8220 inhibited PMA-induced shape changes (nonpolar cells) and pinocytosis, but not fNLPNTL-induced shape changes (polarity) and pinocytosis. At higher concentrations, Ro 31-8220 alone elicited cell polarity and chemokinesis, indicating that a constitutively active protein kinase is involved in maintaining the spherical shape of resting PMNs. Functional effects of another PKC inhibitor, CGP 41,251, on neutrophil function were strikingly different. CGP 41,251 selectively inhibited fNLPNTL-induced polarity and locomotion (but not colchicine or Ro 31-8220-induced polarity), and it failed to inhibit PMA-induced, stimulated pinocytosis and shape changes. Although the effects of Ro 31-8220 vs. CGP 41,251 on PMN function were strikingly different, the inhibition of profiles for constitutive and for fNLPNTL- or PMA-induced protein phosphorylation in intact PMNs showed only small differences, which could not yet be conclusively related to cell function.

Alkaloids↗

PubMed1985

Diclofenac sodium, a negative chemokinetic factor for neutrophil locomotion.

Diclofenac sodium, a non steroidal anti-inflammatory agent, was studied for its influence on the locomotion of human polymorphonuclear neutrophils (PMN), in an attempt to define the mechanism governing the drug's anti-inflammatory properties. PMN locomotion was measured by the agarose technique under two conditions of stimulation of cell migration: in the presence of a gradient of stimuli (chemotaxis) and in the presence of various amounts of stimuli incorporated in the gel (chemokinesis). At concentrations below 10 micrograms/ml, diclofenac in the gel reduced, in a dose-dependent manner, the directed locomotion of PMN induced by a gradient of C5a-activated serum, peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) or Klebsiella pneumoniae culture supernatant (KPCS). Diclofenac also inhibited the random locomotion of unstimulated PMN, as well as the PMN chemokinetic activity induced by various amounts of FMLP or activated serum. Inhibition of PMN locomotion by diclofenac decreased when the concentration of the stimulant was raised; this inhibition was inversely related to the concentration of heat-inactivated fetal calf serum in the medium. The directed locomotion and chemokinesis of PMN, induced by FMLP were also reduced in PMN preincubated with diclofenac before migration, suggesting a direct cellular effect of diclofenac. On the other hand, diclofenac did not affect the changes in shape induced in floating PMN by FMLP or activated serum. The observation that diclofenac did not alter the ingestion rate of bacteria by PMN indicates that this drug is not cytotoxic for PMN. Consequently, diclofenac reduces PMN locomotion by interfering with the PMN chemokinetic activity. Diclofenac is an anti-inflammatory drug possessing the original property of acting as a negative chemokinetic agent, for migration of both stimulated and unstimulated PMN. It should therefore be a useful tool for analyzing the elements controlling PMN locomotion speed.

Blood↗

PubMed1990

Initiation and execution of locomotion elicited by diencephalic stimulation: regional differences in response to nembutal.

At moderate levels of Nembutal, within the anesthetic range, locomotor stepping can be elicited by brain stimulation. We determined if Nembutal (7, 14 and 28 mg/kg) had different effects on locomotion elicited by stimulation at different brain regions. Two regions were compared: the medial forebrain bundle (MFB, 13 sites) and the areas medial and dorsal to it (MED/DORSAL, 20 sites). Locomotion was produced by electrical stimulation (50 microA, 0.5 msec pulses, 10 to 160 Hz) of unrestrained rats in a rotary runway. The latency to initiate locomotion and the time to complete 1 revolution of the rotary were measured. With no drug, MFB locomotion was initiated sooner but took longer to complete than MED/DORSAL locomotion. Nembutal at 7 mg/kg did not affect initiation of MFB or MED/DORSAL locomotion. Nembutal at 14 mg/kg shortened MFB initiations, but this dose prolonged MED/DORSAL initiations. Initiations with both types of sites were blocked with 28 mg/kg. The 7 and 14 mg/kg doses prolonged the locomotor completion times of the MFB sites but not of the MED/DORSAL sites. The results indicate that the response to Nembutal differs qualitatively for locomotion elicited by stimulation of the MFB and locomotion elicited by stimulation of the medial and dorsal hypothalamus. The mechanisms underlying the difference remain to be elucidated; they may relate to nonlocomotor behaviors also elicited by stimulation or to the motivational states reflected in those behaviors.

Animals↗

PubMed2005

Concurrent measures of feeding and locomotion in rats.

Psychostimulants including amphetamine and cocaine induce locomotion and stereotypy and suppress eating. Studies of the biobehavioral actions of psychostimulants commonly focus on locomotion and less commonly on feeding, and only rarely are these measures considered in conjunction within the same animal. Inasmuch as hyperactivity induced by a psychostimulant may compete with other motor behaviors, including eating, it would be important to concurrently assess changes in eating and locomotion after psychostimulant treatment. The present paper describes a modification of an automated activity chamber in which minute-by-minute recordings of food consumption are gathered in parallel with an assessment of locomotion. The present experiment illustrates the method by characterizing the temporal changes in locomotion and eating produced by administration of hypophagic doses of nicotine tartrate (0.28 mg/kg (as the base), IP) or cocaine hydrochloride (7.5 mg/kg, IP). At these doses, nicotine suppressed eating and locomotion, whereas cocaine suppressed eating, but facilitated forward locomotion. These outcomes support the viability of this apparatus and the concurrent method for the dissociation of feeding and locomotion.

Animals↗

PubMed1991

Hyaluronan and a cell-associated hyaluronan binding protein regulate the locomotion of ras-transformed cells.

Hyaluronan (HA) and one of its cell binding sites, fibroblast hyaluronan binding protein (HABP), is shown to contribute to the regulation of 10T1/2 cell locomotion that contain an EJ-ras-metallothionein (MT-1) hybrid gene. Promotion of the ras-hybrid gene with zinc sulfate acutely stimulates, by 6-10-fold, cell locomotion. After 10 h, locomotion drops to two- to threefold above that of uninduced cells. Several observations indicate increased locomotion is partly regulated by HA. These include the ability of a peptide that specifically binds HA (HABR) to reduce locomotion, the ability of HA (0.001-0.1 micrograms/ml), added at 10-30 h after induction to stimulate locomotion back to the original, acute rate, and the ability of an mAb specific to a 56-kD fibroblast HABP to block locomotion. Further, both HA and HABP products are regulated by induction of the ras gene. The effect of exogenous HA is blocked by HABR, is dose-dependent and specific in that chondroitin sulfate or heparan have no significant effect. Stimulatory activity is retained by purified HA and lost upon digestion with Streptomyces hyaluronidase indicating that the activity of HA resides in its glycosaminoglycan chain. Uninduced cells are not affected by HA, HABR, or mAb and production of HA or HABP is not altered during the experimental period. These results suggest that ras-transformation activates an HA/HABP locomotory mechanism that forms part of an autocrine motility mechanism. Reliance of induced cells on HA/HABP for locomotion is transient and specific to the induced state.

Carrier Proteins↗

PubMed1990

Modulation of leucocyte locomotion by interleukin-1.

The influence of interleukin-1 (IL-1) upon leucocyte locomotion in vitro was studied, using either casein or zymosan-activated serum (ZAS) as chemotaxigens. A pre-incubation of polymorphonuclear cells (PMNC) with ultrapure (purity 99%) human IL-1 (1 U/ml) for 2 and 5 h followed by a washing step resulted in a significant decrease in leucocyte locomotion against casein (P less than 0.0005 and P less than 0.01, respectively), but not against ZAS (P greater than 0.1). Moreover, the direct addition of this IL-1 preparation to leucocyte locomotion assays without pre-incubation produced a similar and significant inhibition of leucocyte locomotion directed against casein (P less than 0.05). This inhibitory effect could not be augmented further by higher concentrations of ultrapure IL-1. In order to exclude the effect of possibly contaminating cytokines in the ultrapure IL-1 preparation used, additional assays with recombinant human IL-1 (rIL-1) alpha and rIL-1 beta (1 U/ml) were performed to investigate their influence upon leucocyte locomotion. It was found that both rIL-1 alpha and rIL-1 beta inhibited leucocyte locomotion directed against casein significantly (P less than 0.005). Similar to the previous experiments, leucocyte locomotion could not be further inhibited by higher concentrations (10 U/ml) or rIL-1. Thus, both ultrapure and rIL-1 were found to have the ability to inhibit leucocyte locomotion in vitro.

Caseins↗

PubMed1986

Locomotion and stereotyped behaviours induced by 1-amino-3,5-dimethyladamantane (D 145) and apomorphine in the rat: a comparison.

The locomotion and stereotyped behaviours induced by the two dopamine agonists, 1-amino-3,5-dimethyladamantane (D 145) and apomorphine in rats have been investigated using a holeboard apparatus. Unlike apomorphine, D 145 did not induce compulsive gnawing, but it did induce locomotion dose-dependently. However, the pattern of locomotion was different from that induced by apomorphine and the locomotion itself was potently antagonized by haloperidol but not by sulpiride; this is the opposite to apomorphine-induced locomotion. This indicates that locomotion induced by dopamine agonists is not a unitary phenomenon but that different 'types' of locomotion, with different pharmacological properties, can be induced. Low doses of D 145, given before apomorphine, reduced apomorphine-induced gnawing and enhanced apomorphine-induced locomotion. The long lasting 'priming' effect known to occur after repetitive injections of apomorphine was not mimicked by D 145. Apomorphine and D 145 are considered to be two specific DA agonists; their behavioural-pharmacological profiles, however, are quite different.

Amantadine↗

PubMed2004

Candidate interneurones mediating group I disynaptic EPSPs in extensor motoneurones during fictive locomotion in the cat.

In the present study we sought to find interneurones responsible for the group I-evoked disynaptic excitation of hindlimb extensor motoneurones that occurs during fictive locomotion. Locomotion was produced by stimulation of the mesencephalic locomotor region (MLR) in decerebrate paralysed cats in which activation of ankle extensor group I afferents evoked a disynaptic excitation of motoneurones during the extension phase of fictive locomotion. Extracellular recordings were used to locate interneurones fulfilling all, or five of the six following criteria: (i) weak or no response to stimulation of extensor group I afferents in the absence of locomotion; (ii) strong group I activation during locomotion; (iii) group I activation at monosynaptic latencies; (iv) strong group I activation during only the extensor phase of locomotion; and (v) antidromic activation from the extensor motor nuclei; but (vi) no antidromic activation from rostral spinal segments. Candidate excitatory interneurones were located in mid to caudal parts of the L7 segments in areas where monosynaptic field potentials were evoked by group I afferents, within 2 mm of the stimulation site in the ventral horn from which they were antidromically activated. All were activated during extension by stimulation of group I afferents in extensor nerves. In the absence of peripheral nerve stimulation, six of the seven candidate excitatory interneurones were rhythmically active with maximal activation during the extension phase of fictive locomotion. Rhythmic activity during extension was also seen in five additional interneurones located near candidate interneurones but not activated by group I strength stimulation of the tested nerves. We suggest that the lumbosacral interneurones located in the intermediate laminae that can be activated by extensor group I afferents during the extension phase are a previously unknown population of interneurones, and may mediate group I-evoked disynaptic excitation of extensor motoneurones. Their rhythmic activity suggests that they also provide central excitatory drive to extensor motoneurones during locomotion.

Afferent Pathways↗

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↗

PubMedDate not supplied

Low cost of locomotion in the banded Gecko: a test of the nocturnality hypothesis.

This study tested the hypothesis that there has been an evolutionary increase in locomotor performance capacity at low temperature in nocturnal lizards. Nocturnal lizards are often active at low and suboptimal body temperatures. An evolutionary decrease in the minimum cost of locomotion could increase endurance capacity at low temperature, partially offsetting the thermal handicap of nocturnality. In support of the nocturnality hypothesis, we discovered that minimum cost of locomotion of a nocturnal gecko, Coleonyx variegatus (4.2 g), was only 58% of the minimum cost of locomotion of Phrynosoma douglassii, a diurnal lizard (4.5 g). As a result, maximum aerobic speed was 2.3 times as great in the nocturnal lizard compared to the diurnal lizard. By using the method of phylogenetically independent contrasts at the species level, we showed that the relationship between mass and minimum cost of locomotion in diurnal lizards was similar to that of the ahistorical standard allometry and that low minimum cost of locomotion in geckos represents a significant evolutionary change from the ancestral diurnal pattern. The decrease in the minimum cost of locomotion concordant with the evolution of nocturnality suggests that geckos evolved a greater capacity for sustained locomotion at low temperature.

Animals↗