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Sökning: swepub > Umeå universitet > Refereegranskat > Högskolan i Gävle > Ljubisavljevic Milos

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1.
  • Björklund, Martin, et al. (författare)
  • Muscle stretch-induced modulation of noxiously activated dorsal horn neurons of feline spinal cord.
  • 2004
  • Ingår i: Neuroscience research. - 0168-0102. ; 48:2, s. 175-184
  • Tidskriftsartikel (refereegranskat)abstract
    • The present work was designed to check for the possibility of interactions between mechanical innocuous and chemically induced noxious muscle afferent inputs on discharge behavior of nociceptive superficial dorsal horn neurons (SDHNs) of the spinal cord in decerebrated cats. The innocuous and noxious stimuli were applied separately and in combination, so that the effects of the innocuous stimulus on nociceptive processing could be evaluated. The innocuous stimulus consisted of ramp-and-hold stretches of the gastrocnemius muscles, whereas the noxious stimulus consisted of i.a. injections of bradykinin (BK; 0.5-1 ml, 50 microg/ml) into the arterial circulation of same muscles. Only neurons up to approximately 1mm depth and those that responded to noxious pinch of the gastrocnemius muscles were selected for further analysis. The activity of 16 dorsal horn neurons was recorded extracellularly with high-impedance glass microelectrodes, out of which seven responded to stretch, while 12 neurons responded to bradykinin injections. The bradykinin injections induced three types of responses: excitatory, inhibitory and mixed. The majority of the neurons that showed excitatory and mixed responses to bradykinin were also influenced by stretches applied directly after the bradykinin injection. In these neurons, the stretch usually counteracted the bradykinin-induced response, i.e. shortening and reducing bradykinin-induced excitation and re-exciting the cells after bradykinin-induced inhibition. The mechanism of the stretch modulation is proposed to reside in a segmental spinal control of the nociceptive transmission.
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2.
  • Kalezic, Ivana, et al. (författare)
  • Fatigue-related depression of the feline monosynaptic gastrocnemius-soleus reflex
  • 2004
  • Ingår i: Journal of Physiology. - London : Cambridge U. P.. - 0022-3751. ; 556:1, s. 293-296
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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3.
  • Korotkov, Alexander, et al. (författare)
  • Comparison of brain activation after sustained non-fatiguing and fatiguing muscle contraction : a positron emission tomography study.
  • 2005
  • Ingår i: Experimental Brain Research. - 0014-4819. ; 163:1, s. 65-74
  • Tidskriftsartikel (refereegranskat)abstract
    • The concept of fatigue refers to a class of acute effects that can impair motor performance, and not to a single mechanism. A great deal is known about the peripheral mechanisms underlying the process of fatigue, but our knowledge of the roles of the central structures in that process is still very limited. During fatigue, it has been shown that peripheral apparatus is capable of generating adequate force while central structures become insufficient/sub-optimal in driving them. This is known as central fatigue, and it can vary between muscles and different tasks. Fatigue induced by submaximal isometric contraction may have a greater central component than fatigue induced by prolonged maximal efforts. We studied the changes in regional cerebral blood flow (rCBF) of brain structures after sustained isometric muscle contractions of different submaximal force levels and of different durations, and compared them with the conditions observed when the sustained muscle contraction becomes fatiguing. Changes in cortical activity, as indicated by changes in rCBF, were measured using positron emission tomography (PET). Twelve subjects were studied under four conditions: (1) rest condition; (2) contraction of the m. biceps brachii at 30% of MVC, sustained for 60 s; (3) contraction at 30% of MVC, sustained for 120 s, and; (4) contraction at 50% of MVC, sustained for 120 s. The level of rCBF in the activated cortical areas gradually increased with the level and duration of muscle contraction. The fatiguing condition was associated with predominantly contralateral activation of the primary motor (MI) and the primary and secondary somatosensory areas (SI and SII), the somatosensory association area (SAA), and the temporal areas AA and AI. The supplementary motor area (SMA) and the cingula were activated bilaterally. The results show increased cortical activation, confirming that increased effort aimed at maintaining force in muscle fatigue is associated with increased activation of cortical neurons. At the same time, the activation spread to several cortical areas and probably reflects changes in both excitatory and inhibitory cortical circuits. It is suggested that further studies aimed at controlling afferent input from the muscle during fatigue may allow a more precise examination of the roles of each particular region involved in the processing of muscle fatigue.
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4.
  • Thunberg, Johan, et al. (författare)
  • Brain processing of tonic muscle pain induced by infusion of hypertonic saline.
  • 2005
  • Ingår i: European Journal of Pain. - 1090-3801. ; 9:2, s. 185-94
  • Tidskriftsartikel (refereegranskat)abstract
    • Most of the previous studies on the effects of pain on Regional Cerebral Blood Flow (rCBF) had been done with brief cutaneous or intramuscular painful stimuli. The aim of the present study was to investigate the effect on rCBF of long lasting tonic experimental muscle pain. To this end we performed PET investigations ofrCBF following tonic experimentallow back pain induced by continuous intramuscular infusion ofhypertonic (5%) saline (HS) with computer controIled infusion pump into the right erector spinae on L3 level in 19 healthy volunteers. Changes in rCBF were measured with the use of 150 labelled water during four conditions: Baseline (before start of infusion), Early Pain (4 min after start of infusion), Late Pain (20 min after start of infusion) and Post Pain (> 15 min after stop of infusion) conditions.Results of S PM analysis showed relative rCBF increase in the right insula and bilateral decrease in the temporo-parieto-occipital cortex during initial phase of painful stimulation (Early Pain) followed by activation of the medial prefrontal region and bilateral inhibition ofinsula, anterior cingulat and dorso-lateral prefrontal cortex mainly in ipsilateral hemisphere during Late Pain conditions. The results show that longer lasting tonic experimental muscle pain elicited by i.m infusion ofHS results in decreases rather than increases in rCBF. Possible explanations for differences found in rCBF during tonic hypertonic saline-induced experimental muscle pain as compared with previous findings are discussed.
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