Neuroscience letters
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Neuroscience letters · Jun 2012
Effects of neck flexion on discriminative and cognitive processing in anticipatory postural control during bilateral arm movement.
We investigated the effect of neck flexion on discriminative and cognitive processing in postural control during bilateral arm movement while standing, using event-related potential (ERP) and electromyogram. Fourteen healthy subjects flexed their arms to the target stimuli with a 20% probability in neck resting and flexion positions. Amplitude and latency of N2 and P3, anterior deltoid (AD) reaction time, onset time of postural muscles with respect to AD activation, and peak amplitude and latency of all muscles were measured. ⋯ Significant positive correlations were found in changes with neck flexion between P3 latency and AD reaction time, and between N2 latency and onset time of erector spinae. These suggest that with neck flexion, attention allocation to discriminative and cognitive processing increased, and the processing speed increased with shortening of reaction time in focal muscles. In addition, the onset time of postural muscles became earlier without changing the activation pattern, which was associated with the hastened discriminative processing.
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Neuroscience letters · Jun 2012
Inhibition of EphA4 signaling after ischemia-reperfusion reduces apoptosis of CA1 pyramidal neurons.
Hippocampal CA1 pyramidal neurons are sensitive to ischemic damage. However, the cellular and molecular mechanisms underlying neuronal cell death caused by ischemia-reperfusion (I/R) are not completely clear. ⋯ Blocking ephrinA3/EphA4 interaction by EphA4-Fc, an inhibitor of EphA4, attenuated apoptotic neuronal cell death, likely through the inhibition of caspase-3 activation. These results reveal a novel function of ephrin/Eph signaling in the regulation of apoptosis in CA1 pyramidal neurons after I/R.
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Neuroscience letters · Jun 2012
Inflammatory mediators potentiate high affinity GABA(A) currents in rat dorsal root ganglion neurons.
Following acute tissue injury action potentials may be initiated in afferent processes terminating in the dorsal horn of the spinal cord that are propagated back out to the periphery, a process referred to as a dorsal root reflex (DRR). The DRR is dependent on the activation of GABA(A) receptors. The prevailing hypothesis is that DRR is due to a depolarizing shift in the chloride equilibrium potential (E(Cl)) following an injury-induced activation of the Na(+)-K(+)-Cl(-)-cotransporter. ⋯ This effect was dependent on the concentration of GABA, manifest only at low concentrations (<10 μM). THIP evoked current were also potentiated by IM and GABA (1 μM) induced tonic currents enhanced by IM were resistant to gabazine (20 μM). The present data are consistent with the hypothesis that an acute increase in I(GABA) contributes to the emergence of injury-induced DRR.