Neuroscience letters
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Neuroscience letters · Sep 1993
Capsaicin-induced central facilitation of a nociceptive flexion reflex in humans.
The effect of selective activation of nociceptive primary afferent fibers by capsaicin on a nociceptive lower limb flexion reflex was studied in healthy human subjects. Capsaicin (1%) applied topically to the skin produced a burning spontaneous pain sensation and allodynia in the treated region and in its immediate vicinity. Capsaicin applied to the distal innervation area of the sural or saphenous nerve produced a significant decrease of the threshold for the nociceptive limb flexion reflex induced by electric stimulation of the proximal sural nerve trunk, and this threshold decrease was rapidly attenuated by a cool compress concomitantly with the attenuation of the capsaicin-induced spontaneous pain. ⋯ The non-nociceptive H-reflex was not modified by capsaicin. It is concluded that a selective activation of nociceptive primary afferent fibers of the skin by capsaicin produces a central facilitation of a nociceptive flexion reflex in humans. This facilitation is selective on the nociceptive reflex and depends, at least partly, on the on-going afferent barrage in C-fibers.
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Neuroscience letters · Sep 1993
MK-801, an N-methyl-D-aspartate receptor antagonist, blocks quinolinic acid-induced lipid peroxidation in rat corpus striatum.
In this study, we evaluate the possible participation of lipid peroxidation (LP) in the neurotoxic events that follow after quinolinic acid (QUIN) microinjection into the rat corpus striatum. Two hours after QUIN (240 nmol/microliters) intrastriatal administration, lipid peroxidation was found increased by 32% vs. control as measured by thiobarbituric acid-reactive substances (TBARS). ⋯ The increase of QUIN-induced lipid peroxidation was completely abolished by pretreatment of rats with an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (10 mg/kg, i.p.), 60 min before QUIN microinjection. Results suggest an NMDA receptor involvement in the QUIN-induced oxidative processes.