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- Andrew, Churchill, et al.
(författare)
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Vision of the hand and environmental context in human prehension
- 2000
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Ingår i: Experimental Brain Research. - : Springer Science and Business Media LLC. - 0014-4819 .- 1432-1106. ; 134:1, s. 81-89
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Tidskriftsartikel (refereegranskat)abstract
- Previous findings on the role of visual contact with the hand in the control of reaching and grasping have been contradictory. Some studies have shown that such contact is largely irrelevant, while more recent ones have emphasised its importance. In contrast, information arising from the surrounding environment has received relatively little attention in the study of prehensile actions. In order to identify the roles of both sources of information, we made kinematic comparisons between three conditions. In the first, reaching was performed in a dimly lit room and compared with a second condition in which reaches in the dark, but with the thumb and first finger illuminated, were made to a luminous object. This contrast allows the effects of environmental context to be identified. A comparison between the second and a third condition, in which both vision of the hand and the environment was removed, but the object was still visually available, enabled the assessment of how and when vision of the hand plays a role. Removing environmental cues had effects both early and late in the reach, while vision of the hand was only crucial in the period after peak deceleration. In addition, removal of both sources of information resulted in larger grip apertures. Differences and similarities between our findings and those of other studies are discussed, as is the ongoing debate about the relative importance of visual feedback of the hand in the control and co-ordination of prehensile actions. We conclude with suggestions for further research based on the set-up used in the present study.
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| 5. |
- Domkin, Dmitry, et al.
(författare)
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Structure of joint variability in bimanual pointing tasks
- 2002
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Ingår i: Experimental Brain Research. - : Springer Science and Business Media LLC. - 0014-4819 .- 1432-1106. ; 143, s. 11-23
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Tidskriftsartikel (refereegranskat)abstract
- Changes in the structure of motor variability during practicing a bimanual pointing task were investigated using the framework of the uncontrolled manifold (UCM) hypothesis. The subjects performed fast and accurate planar movements with both arms, one moving the pointer and the other moving the target. The UCM hypothesis predicts that joint kinematic variability will be structured to selectively stabilize important task variables. This prediction was tested with respect to selective stabilization of the trajectory of the endpoint of each arm (unimanual control hypotheses) and with respect to selective stabilization of the timecourse of the vectorial distance between the target and the pointer tip (bimanual control hypothesis). Components of joint position variance not affecting and affecting a mean value of a selected variable were computed at each 10% of normalized movement time. The ratio of these two components ( R(V)) served as a quantitative index of selective stabilization. Both unimanual control hypotheses and the bimanual control hypothesis were supported both prior to and after practice. However, the R(V) values for the bimanual control hypothesis were significantly higher than for either of the unimanual control hypothesis, suggesting that the bimanual synergy was not simply a simultaneous execution of two unimanual synergies. After practice, an improvement in both movement speed and accuracy was accompanied by counterintuitive changes in the structure of kinematic variability. Components of joint position variance affecting and not affecting a mean value of a selected variable decreased, but there was a significantly larger drop in the latter when applied on each of the three selected task variables corresponding to the three control hypotheses. We conclude that the UCM hypothesis allows quantitative assessment of the degree of stabilization of selected performance variables and provides information on changes in the structure of a multijoint synergy that may not be reflected in its overall performance.
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| 8. |
- Hammar, Ingela, 1964, et al.
(författare)
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A comparison of postactivation depression of synaptic actions evoked by different afferents and at different locations in the feline spinal cord.
- 2002
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Ingår i: Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. - : Springer Science and Business Media LLC. - 0014-4819. ; 145:1, s. 126-9
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Tidskriftsartikel (refereegranskat)abstract
- Postactivation depression of synaptic actions of group I and II muscle afferents and low threshold cutaneous afferents was compared with depression of actions of group Ia afferents on alpha-motoneurones in cats deeply anaesthetised with pentobarbital and alpha-chloralose. The depression was analysed on field potentials (population EPSPs). The degree of depression was evaluated by analysing changes in the monosynaptic components of the field potentials, in areas within 0.4- to 0.6-ms-long time windows from their onset. When intervals between successive stimuli used to evoke field potentials were reduced from 10 s to 0.4 s, the potentials evoked by Ia afferents in motor nuclei were depressed as described previously. Field potentials evoked by group II afferents and cutaneous afferents in the dorsal horn were similarly depressed. In contrast, monosynaptic components of field potentials evoked in the intermediate zone, by group I or II afferents, were only marginally affected. Postactivation depression of synaptic actions of group I afferents in the intermediate zone was not enhanced when test stimuli were applied 30-40 ms after a train of four conditioning stimuli. These observations indicate that the degree of postactivation depression may differ depending on the type of afferent. In addition, if postactivation depression depends on intrinsic properties of afferent terminals, differences in the degree of depression of postsynaptic potentials evoked by the same group of afferents at different locations may indicate that properties of terminals contacting different neurones may differ.
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| 9. |
- Hart, Andrew McKay, et al.
(författare)
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Primary sensory neurons and satellite cells after peripheral axotomy in the adult rat : timecourse of cell death & elimination
- 2002
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Ingår i: Experimental Brain Research. - : Springer-Verlag New York. - 0014-4819 .- 1432-1106. ; 142:3, s. 308-318
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Tidskriftsartikel (refereegranskat)abstract
- The timecourse of cell death in adult dorsal root ganglia after peripheral axotomy has not been fully characterised. It is not clear whether neuronal death begins within I week of axotomy or continues beyond 2 months after axotomy. Similarly, neither the timecourse of satellite cell death in the adult, nor the effect of nerve repair has been described. L4 and L5 dorsal root ganglia were harvested at 1-14 days, 1-6 months after sciatic nerve division in the adult rat, in accordance with the Animals (Scientific Procedures) Act 1986. In separate groups the nerve was repaired either immediately or following a 1-week delay, and the ganglia were harvested 2 weeks after the initial transection. Microwave permeabilisation and triple staining enabled combined TUNEL staining, morphological examination and neuron counting by the stereological optical dissector technique. TUNEL-positive neurons, exhibiting a range of morphologies, were seen at all timepoints (peak 25 cells/group 2 weeks after axotomy) in axotomised ganglia only. TUNEL-positive satellite cell numbers peaked 2 months after axotomy and were more numerous in axotomised than control ganglia. L4 control ganglia contained 13,983 (SD 568) neurons and L5, 16,285 (SD 1,313). Neuron loss was greater in L5 than L4 axotomised ganglia, began at I week (15%, P=0.045) post-axotomy, reached 35% at 2 months (P<0.001) and was not significantly greater at 4 months or 6 months. Volume of axotomised ganglia fell to 19% of control by 6 months (P<0.001). In animals that underwent nerve repair, both the number of TUNEL-positive neurons and neuron loss were reduced. Immediate repair was more protective than repair after a 1-week delay. Thus TUNEL positivity precedes actual neuron loss, reflecting the time taken to complete cell death and elimination. Neuronal death begins within I day of peripheral axotomy, the majority occurs within the first 2 months, and limited death is still occurring at 6 months. Neuronal death is modulated by peripheral nerve repair and by its timing after axotomy. Secondary satellite cell death also occurs, peaking 2 months after axotomy. These results provide a logical framework for future research into neuronal and satellite cell death within the dorsal root ganglia and provide further insight into the process of axotomy induced neuronal death.
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| 10. |
- Hart, Andrew McKay, et al.
(författare)
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Systemic acetyl-L-carnitine eliminates sensory neuronal loss after peripheral axotomy : a new clinical approach in the management of peripheral nerve trauma
- 2002
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Ingår i: Experimental Brain Research. - : Springer-Verlag New York. - 0014-4819 .- 1432-1106. ; 145:2, s. 182-189
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Tidskriftsartikel (refereegranskat)abstract
- Several hundred thousand peripheral nerve injuries occur each year in Europe alone. Largely due to the death of around 40% of primary sensory neurons, sensory outcome remains disappointingly poor despite considerable advances in surgical technique; yet no clinical therapies currently exist to prevent this neuronal death. Acetyl-L-carnitine (ALCAR) is a physiological peptide with roles in mitochondrial bioenergetic function, which may also increase binding of nerve growth factor by sensory neurons. Following unilateral sciatic nerve transection, adult rats received either one of two doses of ALCAR or sham, or no treatment. Either 2 weeks or 2 months later, L4 and L5 dorsal root ganglia were harvested bilaterally, in accordance with the Animal (Scientific Procedures) Act 1986. Neuronal death was quantified with a combination of TUNEL [TdT (terminal deoxyribonucleotidyl transferase) uptake nick end labelling] and neuron counts obtained using the optical disector technique. Sham treatment had no effect upon neuronal death. ALCAR treatment caused a large reduction in the number of TUNEL-positive neurons 2 weeks after axotomy (sham treatment 33/group; low-dose ALCAR 6/group, P=0.132; high-dose ALCAR 3/group, P<0.05), and almost eliminated neuron loss (sham treatment 21%; low-dose ALCAR 0%, P=0.007; high-dose ALCAR 2%, P<0.013). Two months after axotomy the neuroprotective effect of high-dose ALCAR treatment was preserved for both TUNEL counts (no treatment five/group; high-dose ALCAR one/group) and neuron loss (no treatment 35%; high-dose ALCAR -4%, P<0.001). These results provide further evidence for the role of mitochondrial bioenergetic dysfunction in post-traumatic sensory neuronal death, and also suggest that acetyl-L-carnitine may be the first agent suitable for clinical use in the prevention of neuronal death after peripheral nerve trauma.
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