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Energy balance of human locomotion in water.

In this paper a complete energy balance for water locomotion is attempted with the aim of comparing different modes of transport in the aquatic environment (swimming underwater with SCUBA diving equipment, swimming at the surface: leg kicking and front crawl, kayaking and rowing). On the basis of the values of metabolic power (E), of the power needed to overcome water resistance (Wd) and of propelling efficiency (etaP=Wd/Wtot, where Wtot is the total mechanical power) as reported in the literature for each of these forms of locomotion, the energy cost per unit distance (C=E/v, where v is the velocity), the drag (performance) efficiency (etad=Wd/E) and the overall efficiency (etao=Wtot/E=etad/etaP) were calculated. As previously found for human locomotion on land, for a given metabolic power (e.g. 0.5 kW=1.43 l.min(-1) VO2) the decrease in C (from 0.88 kJ.m(-1) in SCUBA diving to 0.22 kJ.m(-1) in rowing) is associated with an increase in the speed of locomotion (from 0.6 m.s(-1) in SCUBA diving to 2.4 m.s(-1) in rowing). At variance with locomotion on land, however, the decrease in C is associated with an increase, rather than a decrease, of the total mechanical work per unit distance (Wtot, kJ.m(-1)). This is made possible by the increase of the overall efficiency of locomotion (etao=Wtot/E=Wtot/C) from the slow speeds (and loads) of swimming to the high speeds (and loads) attainable with hulls and boats (from 0.10 in SCUBA diving to 0.29 in rowing).

Algorithms↗

Effect of noradrenaline and 5-hydroxytryptamine depletion on locomotion in the cat.

It has recently been hypothesized that stimulation of the mesencephalic locomotor region (MLR) can give rise to locomotion in mesencephalic cats due to activation of descending monoaminergic pathways to the spinal cord. This notion is based on the findings that monoamine agonists and precursors can induce hindlimb stepping in acute low spinal animals, and on the similarities between the effects of the noradrenaline (NA) precursor, L-DOPA, and stimulation of the MLR. The hypothesis that the descending monoamine systems comprise the only pathways which control the initiation of locomotion has been tested in the present study. NA was depleted from the CNS using intraspinal and intraventricular injections of 6-hydroxydopamine and i.v. injections of the NA synthesis inhibitor, alpha-methyltyrosine. Depletion of 5-hydroxytryptamine (5-HT) was achieved using intraventricular injections of 5,6-dihydroxytryptamine and i.p. p-chlorophenylalanine. These treatments did not abolish evoked locomotion in spite of substantial depletion of NA and 5-HT in the spinal cord and brain stem (maximal depletions of NA up to 14% of control in lumbar cord and 16% of control in pons; maximal depletions of 5-HT up to 19% of control in sacral cord and 25% of control in medulla). Combined depletion of NA and 5-HT did not abolish evoked locomotion in mesencephalic cats, although the treated animals displayed pronounced ataxia prior to decerebration. Depletion of NA or 5-HT alone did not alter locomotion in otherwise intact animals. A previous report that phenoxybenzamine antagonizes the effects of MLR stimulation was not confirmed. The results therefore do not support the hypothesis that descending pathways containing monoamines are essential for locomotion evoked by brain stem stimulation.

5,7-Dihydroxytryptamine↗

The role of putative excitatory amino acid neurotransmitters in the initiation of locomotion in the lamprey spinal cord. I. The effects of excitatory amino acid antagonists.

The activation of N-methyl-D-aspartate (NMDA) and kainate receptors will evoke fictive locomotion in the appropriate motor pattern for locomotion in the isolated lamprey spinal cord, but not a selective activation of quisqualate receptors. The present experiments test whether the initiation of locomotion in response to sensory stimulation depends on these types of receptors. An in vitro preparation of the lamprey spinal cord with part of its tailfin left innervated has been used. In this preparation a sequence of fictive locomotion (i.e. alternating bursts in the segmental ventral roots with a rostrocaudal phase lag) can be elicited by continual sensory stimulation of the tailfin. The effects of excitatory amino acid antagonists were studied by recordings from ventral roots (extracellularly) and motoneurones (intracellularly). It was found that the strong initial bursts of each swimming sequence induced by sensory stimulation were depressed by combined NMDA/kainate antagonists (cis-2,3-piperidine dicarboxylate (PDA) and gamma-D-glutamylglycine (gamma-DGG] whereas the less intense burst activity, occurring particularly towards the end of each swimming sequence, was depressed by a selective NMDA antagonist, 2-amino-5-phosphonovalerate (2-APV). This condition could be mimicked in an isolated spinal cord preparation by an application of L-glutamate; the low-level fictive locomotion induced by low doses of L-Glu (less than 100 microM) was depressed by a NMDA antagonist (2-APV), and, if higher doses were applied, the activity was only depressed by PDA/gamma-DGG. The mode and time course of the depression (by excitatory amino acid antagonists) of fictive locomotion, induced by sensory stimulation, shows that the putative excitatory amino acid neurotransmitter directly or indirectly acts at the pattern generating circuitry within the spinal cord.

Amino Acids↗

Effects of magnesium on fictive locomotion induced by activation of N-methyl-D-aspartate (NMDA) receptors in the lamprey spinal cord in vitro.

It has previously been demonstrated that an activation of N-methyl-D-aspartate (NMDA) receptors can induce fictive locomotion as well as tetrodotoxin (TTX)-resistant membrane potential oscillations in certain types of neurones in the in vitro preparation of the lamprey spinal cord. These oscillations in individual neurones depend on voltage-sensitive properties of NMDA-activated channels which are only manifested in the presence of Mg2+. To evaluate the role of these pacemaker-like oscillations in the generation of locomotion, the motor patterns induced by N-methyl-D,L-aspartate (NMA) before and after removal of Mg2+ were compared. It was found that the ventral root burst pattern of fictive locomotion was more irregular after removal of Mg2+, particularly at low burst rates. This suggests that the membrane properties underlying the NMDA-induced TTX-resistant membrane potential oscillations are of importance for the generation of a stable and regular locomotor activity in particular at low rates of fictive locomotion. When fictive locomotion was induced instead by an activation of kainate receptors a removal of Mg2+ had no effect on the motor pattern. The effects of the two K+-channel blockers, tetraethylammonium (TEA) and gallamine were also tested on NMA-induced fictive locomotion. Both compounds caused an increase in the burst frequency. The Mg2+-dependent NMDA-induced bistable membrane properties thus appear to be of importance for the operation of the network which generates the locomotor pattern.

Animals↗

Effects of corticotropin-releasing factor (CRF) and opiates on amphibian locomotion.

Male rough-skinned newts (Taricha granulosa) were used as a model for the study of the neuroendocrine regulation of locomotion. Intracerebroventricular (i.c.v.) injections of nanogram quantities of corticotropin-releasing factor (CRF) dose-dependently increased locomotion as measured in a circular open-field test arena. In other studies animals received intraperitoneal (i.p.) injections of saline or naloxone, a synthetic opioid antagonist, followed by i.c.v. injections of saline or CRF. With 1-min intervals between injections, neither i.p. saline nor naloxone injections modified the stimulatory effects of CRF injections on locomotor activity. In contrast, with 20-min intervals between injections, the naloxone-plus-CRF injected newts displayed more locomotor activity than the saline-plus-CRF injected newts, suggesting that the opioid system modulated the behavioral effects of CRF. An i.p. injection of bremazocine, an opiate kappa-receptor agonist, suppressed spontaneous locomotion but not CRF-induced locomotion. In contrast, an i.p. injection of morphine, an opiate mu-receptor agonist, did not affect spontaneous locomotion but reduced CRF-induced locomotion, indicating further that the opioid system may modulate the behavioral effects of CRF in this amphibian. The present study provides the first evidence that both CRF and opioids may be involved in the regulation of amphibian locomotor activity.

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Stimulant-conditioned locomotion is not affected by blockade of D1 and/or D2 dopamine receptors during conditioning.

A series of experiments were conducted to investigate the role of dopamine (DA) D1 and D2 receptor subtypes in stimulant-conditioned locomotion in rats. Expt. 1 demonstrated that locomotion could be induced by a testing situation when that situation was previously paired with (+)-amphetamine (1.5 mg/kg, s.c.) or a D2 receptor selective agonist (PHNO, 15 or 30 micrograms/kg, s.c.), but not when the drug treatments were given 3 h after exposure to the situation. The selective D2 receptor antagonist, haloperidol (50 micrograms/kg, i.p.), and the D1 receptor antagonist, SCH 23390 (20 micrograms/kg, s.c.), blocked amphetamine-induced locomotion during the pairing process, but failed to block amphetamine-conditioned locomotion as assessed during a drug-free test in Expt. 2. This was true when the antagonists were given separately or together. The results of Expts. 3 and 4 showed that doses of the D1 (20 micrograms/kg, s.c.) and D2 antagonist (250 micrograms/kg, i.p.) that blocked the unconditioned locomotor effects of PHNO failed to block its conditioned locomotion. It is concluded that neither D1 nor D2 DA receptors are essential for the development of stimulant-conditioned locomotion.

Amphetamines↗

Activity in the mesencephalic locomotor region during locomotion.

The activity of single neurons in the mesencephalic locomotor region (MLR) was recorded extracellularly in cats during spontaneous locomotion on a treadmill. Although stimulation of the MLR is required to induce locomotion on a treadmill after a precollicular-postmamillary brain stem transection in the cat, spontaneous locomotion may occur after a precollicular-premamillary transection. The activity of flexor and extensor muscles of each limb also was recorded by EMG. Nearly 50% of the MLR neurons exhibited rhythmic firing patterns during locomotion. In about one-half of those cells, unit firing patterns could be correlated with the EMG activity in one or more muscles by using spike-triggered averaging. Single MLR neurons were found to be correlated to EMG activity in a single limb, and others were related to the EMG from muscles in two limbs or in all four limbs. Passive movement or stoppage of the limb(s) did not abolish rhythmicity in these neurons. In addition, somatosensory stimulation did not appear to affect the firing patterns of MLR neurons. Averaged EMGs of correlated forelimb muscles revealed a postspike mean latency of 7.1 ms. These measurements agreed well with reports of a 1- to 1.5-ms delay in MLR projections to reticulospinal neurons and a 5- to 6-ms delay (postspike) in reticulospinal activity correlated to EMGs during locomotion. These findings suggest that (a) MLR neurons are rhythmically active during locomotion, (b) the activity of MLR neurons can be correlated with that of EMGs in one or more limbs, (c) rhythmicity in MLR neurons may be independent of phasic sensory input, and (d) the downstream influence of the MLR may be relayed, at least in part, via reticulospinal neurons.

Animals↗

Increased open field locomotion and decreased striatal GABAA binding after activity wheel running.

Open-field behavior has been used to model reductions in anxiety-related behaviors in the rat after chronic physical activity. Plausible mechanisms for the increased open field locomotion observed after physical activity have not been studied. Open field locomotion is decreased by gamma-aminobutyric acid (GABA) and its agonists, and increased by GABA antagonists, in the ventral striatum. Hence, we tested the hypothesis that increased open field locomotion following chronic physical activity would be accompanied by a decrease in the number of GABAA receptors in the corpus striatum. Young (approximately 55 days) male Sprague-Dawley rats (N = 24) were randomly assigned to three conditions: 24-h access to an activity wheel (AW), running for 1 h without shock 6 days/week on a motorized treadmill (TM), or sedentary control (C). Open field locomotion (total and center squares traversed), defecation, and urination were assessed on each of 3 consecutive days prior to and again after 8 weeks of physical activity. Open field locomotion (total and center squares) increased after activity wheel running, decreased after treadmill training, and did not change for control animals. GABAA receptor density indicated by [3H] bicuculline binding (fmol/mg) was lower for activity wheel animals compared with treadmill animals and controls. GABA concentration (mumol/g) was not different between activity wheel and treadmill groups but was higher for both groups contrasted with controls. Our findings of decreased GABAA density in the corpus striatum concomitant with an increase in open field locomotion are consistent with an anxiolytic effect of chronic activity wheel running.

Animals↗

Effect of forced locomotion on the rest-activity cycle of the cockroach.

Many insects are known to exhibit clear circadian rest-activity rhythms. Attention has focussed more on active behaviors such as locomotion than on rest. I investigated the consequences of disturbances of the rest period on activity states of the cockroach Leucophea maderae. The 24-h rest-activity rhythm of individual animals maintained under a 12 h light-12 h dark schedule was continuously recorded by timelapse video recording. Three activity states were scored: locomotion, immobility, and limb or antenna movements without locomotion. The effect of (i) 3 h forced activity; and of (ii) handling and a new environment was studied. Forced activity during the last 3 h of the light period caused a significant reduction of locomotion, and of limb or antenna movements; and an enhancement of immobility in the first hours of the dark period. However, over the entire 12 h dark period, these parameters did not differ from control. Brief handling in conjunction with a change in environment during the last 3 h of the dark period, was followed by similar, though smaller changes in locomotion as seen after forced locomotion. The results indicate that the time spent in immobility corresponds to a resting state which is regulated as a function of prior activity. Thus immobility in an invertebrate may exhibit similar regulating mechanisms as rest or sleep in vertebrates.

Animals↗

Midbrain stimulation in the anesthetized rat: direct locomotor effects and modulation of locomotion produced by hypothalamic stimulation.

The midbrain contains circuits that modulate locomotion. To delineate some of the involved regions, low-level stimulation (25 microA, 10 s train of 0.5 ms pulses at 50 Hz) was applied to the midbrain during locomotor stepping. Stepping was elicited in the anesthetized (pentobarbital, 40 mg/kg) rat by stimulating the hypothalamus with 0.5 ms pulses at 40 Hz at various currents. The rat was held in a stereotaxic apparatus such that locomotor stepping movements turned a wheel. Facilitation of locomotion was produced by stimulation in the anterior ventromedial midbrain and in the posterodorsal midbrain. When presented alone, such stimulation produced locomotion. Inhibition of locomotion was produced by stimulation of the superior colliculus (ventral layers) and the ventromedial midbrain. Additional inhibitory sites were found in the central gray and the lateral tegmentum. Inhibitory collicular stimulation, when presented alone, was characterized by the absence of any hindlimb response. Inhibitory ventromedial stimulation, when presented alone, frequently produced poststimulation locomotion and when presented with hypothalamic stimulation was characterized by postinhibitory increases in locomotion. These results indicate that: (1) the locomotor effects of stimulation in midbrain and hypothalamic sites can summate: (2) multiple locomotor suppressive systems are present in the midbrain and among them are a collicular system and a ventromedial system.

Animals↗

Interaction between the caudal brainstem and the lamprey central pattern generator for locomotion.

Because of its remarkable simplicity and the robustness of the isolated preparation, the lamprey has been used as a model system to study locomotion and its central pattern generator. The function of the spinal cord is relatively well understood in this context, but the role of the brain or even the caudal brainstem remains less so. We here present a study of the interaction between the caudal brainstem and the spinal pattern generator for locomotion. We show that the interaction is highly complex, with both feedforward input from the brainstem to spinal cord and feedback input from the spinal cord to brainstem playing a significant role in the motor output during locomotion. The brainstem, when diffusely stimulated pharmacologically, can initiate fictive locomotion, or it can disrupt or alter the ongoing D-glutamate initiated motor output. The nature of the disruptions vary greatly, and can induce generalized irregularity, while the alterations can include accelerating or decelerating of the bursting. All behaviors are displayed with spectrograms of the motor nerve discharge. We also show that the unstimulated brainstem can disrupt as well as slow the bursting, but in a complex fashion. Finally, a slow episodic behavior initiated from the caudal brainstem is also described. This can be elicited either by D-glutamate to the brainstem or by ascending activity from the spinal cord pattern generator. Thus, we demonstrate that the interaction between the brainstem and the spinal cord during the production of locomotion is highly complex. The locomotion that is exhibited by the combined brainstem-spinal cord preparation is extremely variable. This is in striking contrast to the variability of the locomotor output pharmacologically induced in the spinal cord alone. The latter preparation exhibits remarkable regularity, or upon occasion, irregularity, but not the routine irregularity or the systemic up and down changes in frequency seen with the brainstem present. However, the pattern of frequency changes induced by the brainstem is not predictable, and remains to be understood.

Animals↗

Locomotion induced by non-contingent intracranial electrical stimulation: Dopamine dependence and general characteristics.

Intracranial self-stimulation (ICSS) is induced by delivery of electrical stimulation contingent upon a response such as bar pressing. This procedure has been widely used to investigate the brain reward system. Recent investigations, however, have noted that non-contingent electrical stimulation, also called experimenter applied stimulation (EAS), produces a unique set of locomotion behaviors that appear to be related to ICSS, and that these behaviors resemble locomotion similar to those elicited by dopamine enhancing drugs. However, little is known about the general characteristics of EAS-induced locomotion. While ICSS appears to be robust, long lasting, and highly rewarding in that the rat will invest vast amounts of time or energy to obtain the electrical stimulation, these parameters have not been explored for EAS. Moreover, the dopamine dependence of EAS-evoked locomotion is also not firmly established. Thus, the present study investigated dopamine dependence and general characteristics of the EAS-induced locomotion to determine its similarity to ICSS. Results suggested that motor and limbic systems were strongly activated by non-contingent EAS, and that the resulting locomotion was dopamine dependent, robust, continued across long time horizons, and was greater than that evoked by contingent electrical stimulation.

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Weight-bearing locomotion mitigates the progression of post-traumatic knee osteoarthritis in male rodents: A systematic review and meta-analysis.

OBJECTIVE: Although knee post-traumatic osteoarthritis (PTOA) has been associated with altered loading, how weight-bearing (WB) activities should be modulated post-injury to preserve knee health remains unknown. This systematic review and meta-analysis examined the effects of WB locomotion on knee PTOA in rodents to provide insight into potential clinical implications. DESIGN: Studies published in PubMed, Cochrane Library, Embase, and CINAHL through 02/2025 and meeting the following criteria were included: 1) rodents with knee PTOA, 2) compared locomotor exercises (treadmill/wheel) to no exercise, 3) outcome measures of PTOA (OARSI/Mankin OA scores, bone quality, osteophyte condition, cartilage quality/morphology). If significant heterogeneity across studies was observed, locomotion speed, time/number of intervention sessions, frequency and duration of intervention, exercise initiation, follow-up time, animal species, PTOA model were analyzed as potential moderator variables that may influence findings. RESULTS: Twenty-two studies met the criteria, resulting in a total of 156 effect sizes (ESs) for meta-analysis (all males). A positive ES denotes less PTOA. Based on the CAMARADES checklist, 5 studies were ranked low risk of bias and 14 studies were ranked moderate risk of bias. Locomotion significantly reduced PTOA severity evaluated using OARSI/Mankin scores (ES=0.927, 95% CI: [0.590, 1.264]) and improved bone quality (ES=0.379, 95% CI: [-0.023, 0.780]) with substantial heterogeneity across studies. Follow-up analyses indicated that greater ESs for reducing OA scores were associated with a shorter duration of each training session, more training sessions, longer intervention duration, and longer follow-up time (all P≤0.004). Greater ESs for improving bone quality were associated with a longer follow-up time and later exercise initiation post-injury (both P≤0.014). Locomotion resulted in small to moderate but non-significant positive effects for isolated measures assessing osteophyte condition (ES=0.379, 95% CI: [-0.023, 0.780]), cartilage quality (ES=0.430, 95% CI: [-0.034, 0.893]), and cartilage morphology (ES=0.464, 95% CI: [-0.006, 0.934]). CONCLUSION: WB locomotion reduced the overall degree of knee PTOA in male rodents. Composite knee OA scores may be more responsive to exercise interventions than isolated cartilage/osteophyte measures. The benefits of locomotion may be more prominent with a longer follow-up time or with exercise protocols consisting of shorter but more individual sessions and longer overall intervention durations.

Animals↗

Cutaneous reflex activity of the cat forelimb during fictive locomotion.

To investigate mechanisms of rhythmic modulation of cutaneous reflex by the central pattern generator for locomotion, we made intracellular recordings from elbow flexor motoneurons, biceps brachii (Bi) and brachialis (Br), and quantitatively analyzed excitatory postsynaptic potentials (EPSPs) evoked by stimulation of superficial radial (SR) nerves during forelimb fictive locomotion, which was evoked in immobilized, decerebrate cats with the low thoracic spinal cord transected. We found that (1) in both Br and Bi, SR stimulation evoked trisynaptic EPSPs (segmental latencies were 2.10 +/- 0.39 ms for Br and 2.07 +/- 0.93 ms for Bi), (2) the SR-EPSPs of Br and Bi were rhythmically modulated with a similar pattern; the maximal and minimal EPSPs appeared in the flexor and extensor phase, respectively, (3) however, there were differences as follows. In the control state where fictive locomotion was absent, the mean amplitude of SR-EPSPs of Br (4.65 +/- 2.76 mV, n = 14) was much larger than that of Bi (1.25 +/- 1.22 mV, n = 10). During fictive locomotion, the maximum amplitude of SR-EPSPs of Br was 5.63 +/- 1.79 mV (n = 18), and the minimum was 3.82 +/- 1.69 mV (n = 18); that is, the maximum during fictive locomotion was larger or smaller than that of the control, while the minimal were always smaller. In contrast, SR-EPSPs of Bi were modulated over the control level; the maximum was 3.97 +/- 1.71 mV (n = 16) and the minimum was 2.24 +/- 1.11 mV (n = 16), both the maximum and the minimum during locomotion being larger than that of the control. These results may suggest that two mechanisms are involved in the rhythmic modulation, first, cyclic facilitation in the flexor phase, and secondly, cyclic inhibition in the extensor phase. The former was involved in both cases of Bi and Br motoneurons, while the latter would be involved only in the case of Br motoneurons.

Animals↗

Role of cholinergic receptors in locomotion induced by scopolamine and oxotremorine-M.

Mesopontine cholinergic neurons activate dopamine neurons important for reward-seeking and locomotor activity. The present studies tested whether cholinergic receptor blockade in the ventral tegmental area (VTA) altered locomotion induced by scopolamine (3 mg/kg i.p.) or by oxotremorine-M (0.1 microg bilaterally in the VTA). It was predicted that cholinergic blockers in the VTA would attenuate these cholinergic-induced locomotor increases. Locomotor activity was increased by scopolamine and oxotremorine-M administration in all treatments. When dihydro-beta-erythroidine (DHBE), a nicotinic receptor antagonist, was applied in VTA prior to oxotremorine-M, locomotion was reduced to slightly above saline baseline levels, but atropine, a muscarinic antagonist, had no effect. This suggests that the locomotor effect of oxotremorine-M at this dose was mediated mainly via nicotinic, not muscarinic, receptors. Intra-VTA injections of DHBE, however, did not attenuate scopolamine-induced locomotion indicating that scopolamine-induced locomotion is not mediated mainly via VTA cholinergic receptors. In mutant mice with a deletion in the M5 muscarinic receptor gene, scopolamine-induced locomotion was increased versus wild type mice after scopolamine injection. This suggests that the M5 receptor has an inhibitory effect on scopolamine-induced locomotion.

Animals↗

Dynamic patterns in the locomotion and feeding behaviors by the placozoan Trichoplax adhaerence.

The placozoan Trichoplax adhaerence is one of the most primitive multi-cellular organisms, and moves about accompanying perpetual changes in its shape. Changes in position, locomotion velocity and the outer shape of the organism were monitored quantitatively with use of a computer image analysis, and their dynamic patterns in free locomotion and upon feeding were analyzed in terms of non-linear dynamics. The organism changed its behavioral patterns discontinuously in response to various concentrations of yeast extracts (food). (1) At low concentrations, the organism moved fast with perpetual random changes in shape. Both locomotion velocity and shape changes exhibited 1/f fluctuations. (2) At high concentrations, the shape of the organism as well as the locomotion exhibited oscillations with periods of about 8 min. These limit cycle oscillations bifurcated into the period 2 at the highest concentration tested. The organism flattened more strongly and the locomotion was more reduced on the whole at higher concentrations. (3) At the intermediate concentrations, two patterns as monitored above appeared: one pattern continued for a while and switched to the other abruptly. (4) The average square displacement of the organism increased linearly with time in all cases, indicating that the locomotion is a Brownian movement. In this way, the feeding behaviors by the placozoan are organized as successive co-operative transitions among non-linear dynamic states.

Activity Cycles↗

Basal ganglia efferents to the brainstem centers controlling postural muscle tone and locomotion: a new concept for understanding motor disorders in basal ganglia dysfunction.

The present study is designed to elucidate how basal ganglia afferents from the substantia nigra pars reticulata (SNr) to the mesopontine tegmental area of the brainstem contribute to gait control and muscle-tone regulation. We used unanesthetized and acutely decerebrated cats (n=27) in which the striatum, thalamus and cerebral cortex were removed but the SNr was preserved. Repetitive stimulation (50 Hz, 10-60 microA, for 5-20 s) applied to a mesencephalic locomotor region (MLR), which corresponded to the cuneiform nucleus, and adjacent areas, evoked locomotor movements. On the other hand, stimulation of a muscle-tone inhibitory region in the pedunculopontine tegmental nucleus (PPN) suppressed postural muscle tone. An injection of either glutamatergic agonists (N-methyl-D-aspartic acid and kainic acid) or GABA antagonists (bicuculline and picrotoxin) into the MLR and PPN also induced locomotion and muscle-tone suppression, respectively. Repetitive electrical stimuli (50-100 Hz, 20-60 microA for 5-20 s) delivered to the SNr alone did not alter muscular activity. However stimulating the lateral part of the SNr attenuated and blocked PPN-induced muscle-tone suppression. Moreover, weaker stimulation of the medial part of the SNr reduced the number of step cycles and disturbed the rhythmic alternation of limb movements of MLR-induced locomotion. The onset of locomotion was delayed as the stimulus intensity was increased. At a higher strength SNr stimulation abolished the locomotion. An injection of bicuculline into either the PPN or the MLR diminished the SNr effects noted above. These results suggest that locomotion and postural muscle tone are subject to modulation by GABAergic nigrotegmental projections which have a partial functional topography: a lateral and medial SNr, for regulation of postural muscle tone and locomotion, respectively. We conclude that disorders of the basal ganglia may include dysfunction of the nigrotegmental (basal ganglia-brainstem) systems, which consequently leads to the production of abnormal muscle tone and gait disturbance.

Animals↗

Early development of locomotion: significance of prematurity, cerebral palsy and sex.

Data on the development of locomotion during the first two years of life were collected for 128 preterm infants (21 with varying degrees of cerebral palsy) and for 111 healthy term infants. Most stages of locomotion occurred at slightly later ages among the neurologically unimpaired preterm infants than among those born at term (age corrected for prematurity). There was no difference between preterm and term infants with regard to the number and types of pathways of locomotion, or to age at onset and type of first movements through space. By 9.5 months of age, 95 per cent of term infants and 92 per cent of preterm infants showed some ability to move through space. The infants with severe cerebral palsy had considerable delay in the development of locomotion, but this occurred to only a minor extent when the degree of cerebral palsy was mild or moderate. Most stages of locomotion occurred at slightly earlier ages for boys than for girls, but these differences were not significant at any age. The number and types of pathways of locomotion, and types of first movements, were comparable in both sexes.

Cerebral Palsy↗