Neuroscience research
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Neuroscience research · Jun 2015
Modulation of spinal glial reactivity by intrathecal PPF is not sufficient to inhibit mechanical allodynia induced by nerve crush.
Spinal glial reactivity has been strongly implicated in pain that follows peripheral nerve injury. Among the many therapeutic agents that have been tested for anti-allodynia through immune modulation is the atypical methylxanthine propentofylline. ⋯ Microglial/macrophage Iba-1 and astrocytic GFAP expression, increased in the dorsal horn of nerve crushed animals, was, however, effectively attenuated by propentofylline. Effective modulation of spinal glial reactivity is, thus, no assurance for anti-allodynia.
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Neuroscience research · May 2015
Effects of riluzole on respiratory rhythm generation in the brainstem-spinal cord preparation from newborn rat.
The persistent sodium channel is an important pacemaker component in rhythm generation. In the present study, we examined the effects of a persistent sodium channel blocker, riluzole on pre-inspiratory (Pre-I) and inspiratory neurons in the rostral medulla as well as on 4th cervical ventral root (C4)-inspiratory activity in brainstem-spinal cord preparations. Preparations were isolated from postnatal day 0-3 Wistar rats and were superfused with artificial cerebrospinal fluid, equilibrated with 95% O2 and 5% CO2, pH 7.4, at 25-26 °C. ⋯ Under voltage clamp conditions, riluzole suppressed the negative-slope component of Pre-I neurons. Riluzole also depressed the intrinsic burst generation of Pre-I neurons in low calcium and high magnesium solution. Our findings indicate that the burst generation of Pre-I neurons is more sensitive than inspiratory burst generation to riluzole and thus suggested that persistent sodium channels have an important role in the burst generation of Pre-I neurons and are involved in the primary respiratory rhythm generation.
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Neuroscience research · Mar 2015
Motor imagery of voluntary muscle relaxation induces temporal reduction of corticospinal excitability.
Voluntary muscle relaxation is an "active process" requiring cortical activation. However, cortical activation during motor imagery of muscle relaxation has not been well understood. The purpose of this study was to clarify time-dependent changes in corticospinal excitability during the imagery of muscle relaxation. ⋯ Motor evoked potentials (MEPs) were recorded from the right hand and forearm muscles. The MEP amplitudes of the FDI and the synergist temporally decreased after the auditory cue as compared with those present in the resting condition. Our finding indicates that motor imagery of muscle relaxation induces a temporal reduction of the corticospinal excitability related to the targeted muscle.
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Neuroscience research · Mar 2015
Effect of protons on the mechanical response of rat muscle nociceptive fibers and neurons in vitro.
Strong exercise makes muscle acidic, and painful. The stimulus that activates muscle nociceptors in such instance may be protons. Reportedly, however, not many afferents are excited by protons alone. ⋯ Their response magnitude was increased by both pH 6.2 and pH 6.8; in addition the mechanical threshold was lowered by pH 6.2. Decrease in the threshold by pH6.2 was also observed in MA currents. Presently observed sensitization by protons could be involved in several types of ischemic muscle pain, and may also be involved in cardiovascular and respiratory controls during exercise.
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Neuroscience research · Oct 2014
ReviewStructural features of the Nogo receptor signaling complexes at the neuron/myelin interface.
Upon spinal cord injury, the central nervous system axons are unable to regenerate, partially due to the repulsive action of myelin inhibitors, such as the myelin-associated glycoprotein (MAG), Nogo-A and the oligodendrocyte myelin glycoprotein (OMgp). These inhibitors bind and signal through a single receptor/co-receptor complex that comprises of NgR1/LINGO-1 and either p75 or TROY, triggering intracellular downstream signaling that impedes the re-growth of axons. ⋯ It was also recently shown that gangliosides, such as GT1b, mediate receptor/co-receptor binding. In this review, we highlight these studies and summarize our current understanding of the multi-protein cell-surface complexes mediating inhibitory signaling events at the neuron/myelin interface.