Neuroscience letters
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Neuroscience letters · Aug 1999
Externally guided control of static grip forces by visual feedback-age and task effects in 3-6-year old children and in adults.
This study has been devised to examine the visual feedback control of static grip force levels by pinch and by hand grip during pre-school age and in adults. 69 3-6-year old children and 17 adults were asked to establish and hold grip force levels defined by a visual target and feedback on the dominant and non-dominant hand by hand grip and by pinch grip. From 3 to 6 years of age, the time needed to establish requested grip force levels decreased by a third and the precision increased two-fold for hand grip but four-fold for pinch grip; in contrast to younger children, 5-6-year olds showed a marked superiority of 60% for the pinch grip compared to hand grip, decreasing to about 40% in adults. In the case of pinch grip, all individuals had worse results on higher force levels (children: 50%, adults: 32%). ⋯ In contrast to previous findings in anticipatory grip force regulation, externally guided force regulation begins to develop during late nursery age. Specific developmental effects were found for grip style and for the ability to use visual feedback and to change from external to internal (proprioceptive) control, and to a lesser extent for force magnitude but not for hand laterality and gender. The findings are interpreted by different developmental velocities of motor areas which are responsible for force regulation mechanisms and for grip style.
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Neuroscience letters · Aug 1999
Randomized Controlled Trial Clinical TrialInfluence of the N-methyl-D-aspartate antagonist memantine on human motor cortex excitability.
The aim of our study was to investigate the effect of the N-methyl-D-aspartate (NMDA) antagonist memantine on motor excitability in humans. Seven healthy volunteers received memantine or placebo, respectively, over a period of 8 days. ⋯ Intracortical inhibition was enhanced, and intracortical facilitation reduced after memantine ingestion in comparison to placebo, whereas no significant difference could be observed regarding the other neurophysiological parameters. We conclude that the NMDA receptor is involved in the regulation of excitability of intracortical interneuronal circuits.
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Neuroscience letters · Jul 1999
Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy.
We investigated whether interleukin-1 (IL-1), a mediator of inflammatory pain, also plays a role in pain induced by nerve injury. Female C57BL/6-mice with a chronic constrictive injury of one sciatic nerve, an established model of neurogenic hyperalgesia and allodynia, were treated with different doses (10-80 microg) of a neutralizing monoclonal rat antibody to IL-1 receptor I (anti-IL-1RI). ⋯ Degeneration of myelinated fibers was not altered by any of the treatment schedules. We conclude that IL-1 may be a mediator of hyperalgesia after nerve lesion.
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Neuroscience letters · Jul 1999
Is sympathetic sprouting in the dorsal root ganglia responsible for the production of neuropathic pain in a rat model?
Partial peripheral nerve injury often results in neuropathic pain that is aggravated by sympathetic excitation and induces sympathetic nerve sprouting in both the injured nerve and corresponding dorsal root ganglia (DRGs). Presently, the functional mechanisms of the interactions between the sprouting and injured somatic afferents remain uncertain. ⋯ Immuno-histochemical staining with tyrosine hydroxylase (TH) antibody of the injured S1 DRG taken from both groups of rats after behavioral tests revealed that the magnitude of penetration of TH-positive fibers into the S1 DRG was not significantly different between the two groups. These results suggest that sympathetic nerve sprouting in the injured DRG is not a key factor in the development of neuropathic pain.
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Neuroscience letters · Jul 1999
Lidocaine produces a shunt in rat [correction of rats] thalamocortical neurons, unaffected by GABA(A) receptor blockade.
Low concentrations of lidocaine reversibly decrease input resistance and shunt action potentials in neurons of the ventral posterolateral thalamic nucleus (VPL) in vitro. Using differential interference contrast infrared videomicroscopy and whole-cell patch-clamp techniques in rat brain slices, we studied the effects of bicuculline methobromide to test whether the lidocaine-induced shunt in VPL neurons is mediated by GABA(A) receptors. ⋯ Likewise, bicuculline did not affect the shunt-induced reductions of spike-afterhyperpolarizations produced by lidocaine. The results of this study imply that the effects of low lidocaine concentrations in thalamocortical neurons are not mediated by GABA(A) receptors.