Biomedical subjects

H Sveistrup

Publications and source records attributed to H Sveistrup.

5 recordsLinked to original sources

PubMed1998

Development of postural responses during standing in healthy children and children with spastic diplegia.

Studies on the development of balance control show a clear developmental progression of the emergence of organized muscle response patterns, with tonic background muscle activity decreasing and phasic bursts of activity emerging in all three agonist muscles in a synergic group (gastrocnemius-hamstrings-trunk extensors or tibialis anterior-quadriceps-abdominals) just prior to the onset of independent stance. The rudimentary ability to adapt postural responses to changing task conditions is present in children as young as 1 year of age. Older children with spastic diplegia have muscle activation patterns typically seen in normal children who are at the pull-to-stand stage of development, including poorly organized (proximal activated before distal muscles) responses with a high degree of antagonist co-activation. When normal children were asked to stand in a crouched posture like the CP children, the additional constraint caused muscle response patterns to resemble those of CP children, suggesting that differences in balance control in CP children are due to both CNS deficits and biomechanical changes in postural alignment.

Child↗

PubMed1997

Practice modifies the developing automatic postural response.

The purpose of this study was to examine effects of experience with a postural task on components of the automatic postural response including: (1) probability of activation of functionally appropriate postural muscles; (2) number of functionally appropriate postural muscles activated; and (3) onset latencies of functionally appropriate postural muscles in infants. Infants (n=15; age 36-48 weeks old) able to pull themselves into a standing position but not able to walk independently were tested using a postural task requiring the infant to stand and balance, with support, following a forward or backward movement of the support surface (platform perturbation). Infants were tested twice at 5-day intervals. One-half of the infants, the training group, were given intense platform perturbation training on the days between test sessions. Infants in the second group were also brought into the laboratory on the days between test sessions but were not exposed to platform perturbations during those days. Electromyograms of six leg and trunk muscles were recorded during test sessions to provide muscle onset latencies, probability of muscle activation data, and the number of postural muscles activated following a perturbation. Training infants demonstrated significant increases in probability of activating functionally appropriate muscles with tibialis anterior, quadriceps, and abdominal muscles activated in response to backward sway and gastrocnemius muscle in response to forward sway. The number of functionally appropriate postural muscles activated in a single trial also increased in the training group. There were no significant changes in mean postural muscle onset latencies or number of trials with antagonist muscle coactivation for either training or control groups. These findings suggest that during development selective parameters of the automatic postural response are affected by experience with the postural task.

Child Development↗

PubMed1996

Influence of auditory precuing on automatic postural responses.

An experiment was conducted to determine the influence of auditory precuing on posture control. Specifically, the influence of a warning signal on the onset latencies of the gastrocnemius (G) and tibialis anterior (TA) muscles was determined. An audible 50-ms tone was presented to subjects standing on a moveable platform and preceded a perturbation to standing balance by 500 ms. The perturbations were produced by an anterior or posterior translation (3 cm at 30 cm/s) of the support surface. Unilateral electromyographic activity was recorded from G and TA muscles. In the first series of trials (series A), the muscle onset latencies following perturbations with a nondirectionally specific precue, an invalid precue, and no precue were compared. In the second series of trials (series B), muscle onset latencies following perturbations with a directionally specific precue, invalid precue, and no precue perturbations were compared. In series A, mean muscle onset latencies decreased following nondirectionally specific precues during forward and backward platform perturbations; respectively, TA 6% (91 +/- 9 ms to 86 +/- 9 ms) and G 7% (93 +/- 6 ms to 87 +/- 5 ms). During series B, the TA and G muscle onset latencies decreased following directionally specific precues by 10.4% (92 +/- 12 ms to 82 +/- 6 ms) and 9.8% (92 +/- 9 ms to 83 +/- 6 ms), respectively. There were no significant differences between the types of precues. Thus, prior knowledge of a forthcoming balance perturbation reduces postural muscle onset latency times. In addition, specific prior knowledge reduces muscle onset latency time in the same manner as does nonspecific prior knowledge.

Acoustic Stimulation↗

PubMed1996

Ciliary neurotrophic factor: regulation of acetylcholinesterase in skeletal muscle and distribution of messenger RNA encoding its receptor in synaptic versus extrasynaptic compartments.

Several recent studies have shown that the ciliary neurotrophic factor exerts myotrophic effects in addition to its well-characterized neurotrophic actions on various neuronal populations. Since expression of acetylcholinesterase in skeletal muscle has been shown to be regulated by putative yet unknown nerve-derived trophic factors, we tested the hypothesis that the ciliary neurotrophic factor is a neurotrophic agent capable of influencing expression of acetylcholinesterase in adult rat skeletal muscle in vivo. To this end, we first determined the impact of daily ciliary neurotrophic factor administration on expression of acetylcholinesterase in both intact and denervated rat soleus muscles. The results of our experiments indicate that although chronic administration of ciliary neurotrophic factor partially counteracted the atrophic response of soleus muscles to surgical denervation, thus confirming its myotrophic effects, it failed to either increase acetylcholinesterase expression in intact muscles or prevent the decrease normally occurring in seven-day denervated muscles. In fact, acetylcholinesterase messenger RNA and enzyme levels were further reduced by ciliary neurotrophic factor treatment in denervated muscles without significant modifications in the pattern of acetylcholinesterase molecular forms. Conversely, transcript levels of the epsilon subunit of the acetylcholine receptor in intact and denervated soleus muscles treated with the ciliary neurotrophic factor were similar to those observed in their respective counterparts from vehicle-treated animals. In addition, we also determined whether transcripts encoding the receptor for the ciliary neurotrophic factor selectively accumulate in junctional domains of rat skeletal muscle fibres. In contrast to the preferential localization of transcripts encoding acetylcholinesterase and the epsilon subunit of the acetylcholine receptor within the postsynaptic sarcoplasm, messenger RNAs for the ciliary neurotrophic factor receptor appeared homogeneously distributed between junctional and extra-junctional compartments of both diaphragm and extensor digitorum longus muscle fibres, with no compelling evidence for a selective accumulation within the postsynaptic sarcoplasm. These data show that the ciliary neurotrophic factor exerts an inhibitory influence on expression of acetylcholinesterase in muscle fibres. Furthermore, the lack of an effect on expression of the epsilon acetylcholine receptor transcripts indicates that treatment with ciliary neurotrophic factor does not lead to general adaptations in the expression of all synaptic proteins. Given the distribution of transcripts encoding the ciliary neurotrophic factor receptor along multinucleated muscle fibres, we propose a model whereby the ciliary neurotrophic factor, or a related unknown molecule that also utilizes the receptor for the ciliary neurotrophic factor, contributes to the maintenance of low levels of enzyme activity in extrajunctional regions of muscle fibres by acting as a repressor of acetylcholinesterase expression that functions directly or indirectly via a pretranslational regulatory mechanism. Accordingly, these results further highlight the complexity of the regulatory mechanisms presiding over acetylcholinesterase expression in vivo.

Acetylcholinesterase↗

PubMed1995

Chronic enhancement of neuromuscular activity increases acetylcholinesterase gene expression in skeletal muscle.

We determined levels of mRNA encoding acetylcholinesterase (AChE) in muscles of rats subjected to chronic enhancement of neuromuscular activation. After 8 wk of voluntary wheel running, extensor digitorum longus (EDL) muscles displayed a 72% increase in total AChE activity as a result of a selective threefold increase in the G4 content. Soleus muscles, on the other hand, exhibited a 30% decrease in A12 while displaying a small (33%) increase in total AChE activity. These enzymatic adaptations were paralleled by increases in the levels of AChE mRNAs in both EDL (32%; P < 0.03) and soleus (42%; P < 0.02) muscles. In addition, compensatory hypertrophy of the plantaris muscle increased total AChE activity by 75%. This change was reflected by an elevation in all AChE molecular forms with A12 (89%) and A8 (179%) showing the most prominent increases. Similar to exercise-trained muscles, hypertrophied plantaris muscles displayed an increase in AChE transcripts (25%; P < 0.04). These results indicate that increases in neuromuscular activity modulate expression of the AChE gene in vivo and suggest the involvement of pretranslational regulatory mechanisms in the adaptive response of AChE to enhanced neuromuscular activation.

Acetylcholinesterase↗