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Biomedical subjects

Uwe Windhorst

Publications and source records attributed to Uwe Windhorst.

7 recordsLinked to original sources

Movement-dependent positioning errors in human elbow joint movements.

Healthy adult humans performed elbow movements in a horizontal plane under a small external extending torque (2.1-3.3 Nm). Test movements (TMs) consisted of slow ramp-and-hold flexions in the absence of visual feedback, with the target joint angle to be remembered from a preceding conditioning movement (CM). The CM was produced by matching two beams on the monitor screen: (1) command representing the target position (a straight line); and (2) a signal from the sensor of the elbow joint angle. Two kinds of CM were applied, which had the same target position (50 degrees in most experiments) but differed in initial positions: (1) fully extended joint (0 degrees, P1 CMs); (2) flexed joint (100 degrees, P2 CMs). In a group of 25 subjects, the target in TMs was usually overshot, with the position errors depending on the CMs: 2.7 +/- 0.6 degree (mean +/- SEM) for P1 CMs, and 10.9 +/- 0.7 degree (P < 0.001) for P2 CMs. Vibration of the elbow flexors substantially diminished the difference between the position errors, amounting to--0.31 +/- 0.5 degree and 2.33 +/- 0.6 degrees, respectively. It is suggested that the observed position errors resulted from after-effects in the activity of muscle spindles in agonist and antagonist muscles, but influence of differences in dynamic components of the afferent signals during oppositely directed approaches to the target cannot be excluded.

Adult↗

Capsaicin-induced effects on c-fos expression and NADPH-diaphorase activity in the feline spinal cord.

The distribution of c-fos expression and NADPH-diaphorase reactivity in the cervical and lumbar segments after stimulation of the vanilloid receptors in the dorsal neck muscles with capsaicin was studied in cats anaesthetized with alpha-chloralose. After the unilateral intramuscular injection of capsaicin, the mean number of Fos-immunoreactive neurons detected with an avidin-biotin-peroxidase technique was significantly increased in the superficial laminae (I), neck of the dorsal horn (V), and area around the central canal (VII) within both the cervical and lumbar spinal cord. Most Fos-immunoreactive neurons in the cervical spinal cord were giant and small cells. The widespread distribution of Fos-immunoreactive cells throughout the cervical cord within the intermediate zone (VII) coincided with the sites of localization of last-order premotor interneurons and cells of origin of inter-segmental crossed and uncrossed descending propriospinal pathways to the lumbar spinal cord. Fos-immunoreactive neurons were co-distributed with nitric oxide-generating cells at both levels of the spinal cord, although the double-labeled cells were not observed. In conclusion, the analysis of c-fos expression and NADPH-diaphorase reactivity shows that stimulation of vanilloid receptors in the neck muscles can initiate distinctive neuronal plasticity in the cervical (C1-C8) and lumbar (L1-L7) segments, and confirms the anatomical and functional coupling of both regions during processing of nociceptive signals from the dorsal neck muscles.

Animals↗

Effects in feline gastrocnemius-soleus motoneurones induced by muscle fatigue.

Responses of gastrocnemius-soleus (G-S) motoneurones to stretches of the homonymous muscles were recorded intracellularly in decerebrate cats before, during and after fatiguing stimulation (FST) of G-S muscles. Ventral roots (VR) L7 and S1 were cut, and FST was applied to VR S1, a single FST session including 4 to 5 repetitions of 12-s periods of regular 40 s(-1) stimulation. Muscle stretches consisted of several phases of slow sinusoidal shortening-lengthening cycles and intermediate constant lengths. The maximal stretch of the muscles was 8.8 mm above the rest length. Effects of FST on excitatory postsynaptic potentials (EPSPs) and spikes evoked by the muscle stretches were studied in 12 motoneurones from ten experiments. Stretch-evoked EPSPs and firing were predominantly suppressed after FST, with the exception of a post-contraction increase of the first EPSP after FST, which was most likely due to after-effects in the activity of muscle spindle afferents. The post-fatigue suppression of EPSPs and spike activity was followed by restoration within 60-100 s. Additional bouts of FST augmented the intensity of post-fatigue suppression of EPSPs, with the spike activity sometimes disappearing completely. FST itself elicited EPSPs at latencies suggesting activation of muscle spindle group Ia afferents via stimulation of beta-fibres. The suppression of the stretch-evoked responses most likely resulted from fatigue-evoked activity of group III and IV muscle afferents. Presynaptic inhibition could be one of the mechanisms involved, but homosynaptic depression in the FST-activated group Ia afferents may also have contributed.

Animals↗

Fatigue-related depression of the feline monosynaptic gastrocnemius-soleus reflex.

In decerebrate cats, changes in the monosynaptic reflex (MSR) of gastrocnemius-soleus (G-S) motoneurones were studied after fatiguing stimulation (FST) of the G-S muscles. Monosynaptic reflexes were evoked by stimulation of Ia fibres in the G-S nerve and recorded from a filament of ventral root (VR) L7. FST (intermittent 40 s(-1) stimulation for 10-12 min) was applied to the distal part of the cut VR S1. FST reduced MSR amplitudes to 0.64 +/- 0.04 (mean +/-s.e.m.) of the prefatigue values. The suppression remained stable for approximately 25 min and then MSR amplitudes gradually returned towards the normal. To test for the involvement of presynaptic and recurrent inhibition, MSRs were conditioned by stimulation of the nerve to the posterior biceps and semitendinosus (PBSt) muscles or a filament of VR L7, respectively. The intensity of presynaptic inhibition (reduction of the normalized value of MSR amplitude during conditioning) increased from 0.19 +/- 0.02 in prefatigue to 0.44 +/- 0.04 within a 5.3-18.2 min interval after FST, followed by a recovery. In contrast, the intensity of recurrent inhibition first diminished from 0.23 +/- 0.02 in prefatigue to 0.15 +/- 0.01 within 15.6-30.1 min after FST and then gradually recovered. Both primary afferent depolarization and the intensity of antidromic discharges in primary afferents increased with the presynaptic inhibition intensity. These results demonstrate a fatigue-related suppression of Ia excitation of synergistic motoneurones, probably arising from the activation of group III and IV afferents. The effects could in part be due to increased presynaptic inhibition, while recurrent inhibition plays a minor role.

Animals↗

Static and dynamic input-output relations of the feline medial gastrocnemius motoneuron-muscle system subjected to recurrent inhibition: a model study.

The physiological function of spinal recurrent inhibition is still a matter of debate because of the experimental difficulty or impossibility of observing recurrent inhibition at work in normally behaving animals. The purpose of this study was to investigate, by computer simulation, the role of recurrent inhibition in shaping the input-output (I/O) relationships between descending command signals (DCS) as inputs and motoneuron (MN) and Renshaw cell (RC) firing rates and muscle force as outputs. Changing the spatial (topographical) distribution of recurrent inhibition from nonhomogeneous (as in the standard model) to homogeneous did not alter the I/O relationships significantly, while changing the functional distribution related to MN types did. Altering the global gain of recurrent inhibition, as happens naturally in various motor acts, changes the slopes and positions (at high inputs) of the I/O relationships, making recurrent inhibition a suitable means of gain control. Coupling a decrease in recurrent inhibitory gain with an increase in DCS input, as could occur during slow dynamic contractions, would increase the MN and force gains during the act. Short dynamic ramp-and-hold DCS inputs generate MN firing patterns, to which recurrent inhibition contributes interspike-interval variability and damped oscillations, which are related to issues of tremor and its control.

Action Potentials↗

A model of the feline medial gastrocnemius motoneuron-muscle system subjected to recurrent inhibition.

Recurrent inhibition in the mammalian spinal cord is complex, and its functions are not yet well understood. Skeletomotoneurons (alpha-MNs) excite, via recurrent axon collaterals, inhibitory Renshaw cells (RCs), which in turn inhibit alpha-MNs and other neurons. The anatomical and functional structure of the recurrent inhibitory network is nonhomogeneous, and the gain and filtering characteristics of RCs are modulated by inputs circumventing alpha-MNs. This complex organization is likely to play important roles for the discharge and recruitment properties of alpha-MNs. Modeling this system is a way of investigating hypothesized roles for normal functioning including muscle fatigue and different forms of physiological pathological tremor. In this paper, a detailed model including alpha-MNs, RCs, and the muscle fibers innervated by the alpha-MNs is presented. Outlines of the experimental data underlying the model and the modeling philosophy and procedure are presented. Then the behavior of a RC model is compared with experimental data reported in the literature. Model and experimental data agree well for burst responses elicited by synchronous single-pulse activation of different numbers of motor axons. In addition, the static relation between motor-axon activation rate and RC firing rate agree fairly well in model and experiment, and the same applies to the dynamic responses to step changes in motor-axon rate. The ultimate objective is to use this model in probing the role of recurrent inhibition in the control and stability of (isometric) muscular force under normal and altered conditions occurring during fatigue and muscle pain.

Animals↗

NADPH-diaphorase activity and c-fos expression in medullary neurons after fatiguing stimulation of hindlimb muscles in the rat.

In anaesthetised rats, Fos-immunoreactive and NADPH-diaphorase-positive neurons in the medulla and, for comparison, in the spinal cord were studied after fatiguing stimulation of the hindlimb muscles. Following both direct muscle stimulation and L5 ventral root stimulation, fatigue-related c-fos gene expression was most prominent in the dorsal horn of the ipsilateral L2-L5 segments and within the ipsilateral nucleus tractus solitarius, the caudoventrolateral and rostroventrolateral reticular nuclei, and the intermediate reticular nucleus at levels of -14.3 and -13.8 mm, and contralaterally at -13.2 mm caudal to the bregma. The order of intensity of c-fos expression was as follows: nucleus tractus solitarius>caudoventrolateral and rostroventrolateral reticular nuclei>intermediate reticular nucleus>lateral paragigantocellular nucleus. NADPH-diaphorase reactivity was changed in the following sequence: NTS>intermediate reticular nucleus lateral paragigantocellular nucleus>rostroventrolateral reticular nucleus. Fos-immunoreactive neurons were codistributed with NADPH-diaphorase-reactive cells within the dorsomedial and ventrolateral medulla, and double-staining neurons were found in the nucleus tractus solitarius, intermediate reticular nucleus and lateral paragigantocellular nucleus. The patterns of distribution of c-fos expression and NADPH-diaphorase reactivity show that afferent signals arising from fatiguing muscles may activate spinal and medullary neurons which are involved in nociceptive and cardiovascular reflex pathways. The functional role of nitric oxide (NO) in the generation of cardiovascular and somatosensory responses in the medulla during fatigue of skeletal muscles is discussed.

Animals↗