Neuroreport
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To study the conduction velocity of the spinothalamic tract (STT) we delivered CO2 laser pulses, evoking pinprick sensations, to the skin overlying the vertebral spinous processes at different spinal levels from C5 to T10 and recorded evoked potentials (LEPs) in 15 healthy human subjects. These stimuli yielded large-amplitude vertex potentials consisting of a negative wave at a peak latency of about 200 ms followed by a positive wave at a peak latency of about 300 ms. The mean conduction velocity of the STT was 21 m/s, i.e. higher than the reported velocity of the corresponding primary sensory neurons (type II AMH). Because dorsal stimulation readily yields reproducible brain LEPs, we expect this technique to be useful as a diagnostic tool for assessing the level of spinal cord lesions.
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Neglect patients often present with a rightward shift of the direction straight-ahead of body midline. We investigated whether directions ahead of other body parts were similarly shifted or were differentially affected. ⋯ Moreover, the projection of the left hemibody was smaller than the right in all subjects, with and without neglect. This unexpected finding is discussed with regard to other spatial asymmetries observed in normal subjects.
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Human somatosensory evoked potentials (SEP) contain a brief burst of high-frequency wavelets (>400 Hz) presumably reflecting rapidly repeated population spikes of as-yet undetermined origin. To study state-dependent response changes, SEP after electric median nerve stimulation were recorded in six Parkinson's disease patients perioperatively from intrathalamic electrode implants, and in five non-implanted patients from scalp electrodes, before and under propofol narcosis. ⋯ Low-frequency SEP components which underly the burst at thalamic (P16) and cortical level (N20) did not change significantly. This dissociation of bursts indicates neuronal generators showing different sensitivities to propofol narcosis, with a robust thalamic response and a state-dependent cortical contribution, possibly from pyramidal chattering cells and/or inhibitory interneurons.
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Glutamate transporters are essential for the homeostasis of glutamate and normal function of glutamatergic synapses. Their function was shown to be regulated by redox agents and dimerizations that involves redox changes of cysteine residues. ⋯ Among them is the toxin Tx3-4, from the spider Phoneutria nigriventer, which is able to inhibit glutamate uptake in rat hippocampal synaptosomes. Based on results obtained with manipulation of the redox state of cysteine residues in synaptosomes and in Tx3-4, we suggest that the effect of this toxin on glutamate uptake is due to interactions that involve cysteines both in the toxin and in the transporters.
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We examined the impact of spinal cord injury to a depth of 0.5 mm at L1-L2 (upper lumbar cord injury) and in L6-S1 (lower cord injury) in Wistar rats. Upper lumbar cord injury resulted in the disappearance of the motor evoked potential (MEP) of the gastrocnemius muscle during transcranial magnetic stimulation, while the threshold was decreased in rats with lower cord injury. ⋯ In lower cord injury, the pattern of H-response recruitment curves differed from that in controls. Our results indicated that MEP and the spinal reflex are influenced not only by upper lumbar cord injury but also by lower cord injury.