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Bicuculline-sensitive primary afferent depolarization remains after greatly restricting synaptic transmission in the mammalian spinal cord.
J Neurosci
April 2010
Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Primary afferent neurotransmission is the fundamental first step in the central processing of sensory stimuli. A major mechanism producing afferent presynaptic inhibition is via a channel-mediated depolarization of their intraspinal terminals which can be recorded extracellularly as a dorsal root potential (DRP). Based on measures of DRP latency it has been inferred that this primary afferent depolarization (PAD) of low-threshold afferents is mediated by minimally trisynaptic pathways with GABAergic interneurons forming last-order axoaxonic synapses onto afferent terminals.
View Article and Find Full Text PDFSpinal ventral root after-discharges as a pain index: involvement of NK-1 and NMDA receptors.
Brain Res
April 2006
Laboratory of CNS Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Nagoya 467-8603, Japan.
Nociceptive signals are transmitted to the spinal dorsal horn via primary afferent fibers, and the signals induce withdrawal reflexes by activating spinal motoneurons in the ventral horn. Therefore, nociceptive stimuli increase motoneuronal firing and ventral root discharges. This study was aimed to develop a method for the study of pain mechanisms and analgesics by recording ventral root discharges.
View Article and Find Full Text PDFSimple pharmacological test battery to assess efficacy and side effect profile of centrally acting muscle relaxant drugs.
J Pharmacol Toxicol Methods
June 2006
Pharmacological Research Centre, Gedeon Richter Ltd. H-1475, Budapest, 10, POB 27, Hungary.
Introduction: Centrally muscle relaxants (CMRs) are used mainly for treating muscle spasticities of neurological origin, and painful muscle spasms due to rheumatologic conditions. Their use is frequently associated with dose-limiting adverse effects. New drugs with improved side-effect characteristics are badly needed.
View Article and Find Full Text PDF(+/-)-Kavain inhibits veratridine-activated voltage-dependent Na(+)-channels in synaptosomes prepared from rat cerebral cortex.
Neuropharmacology
September 1995
Institute of Naturheilkunde, University Clinics Ulm, Germany.
Kava pyrones are pharmacologically active compounds extracted from Piper methysticum Forst. Because kava pyrones were characterized by their anticonvulsive, analgesic and centrally muscle relaxing action, we investigated the influence of (+/-)-kavain, a synthetic kava pyrone, on veratridine-stimulated increase in intrasynaptosomal Na+ concentration ([Na+]i) of rat cerebrocortical synaptosomes. [Na+]i was measured spectrofluorometrically employing SBFI as Na+ sensitive fluorescence dye.
View Article and Find Full Text PDFPossible NMDA antagonist properties of drugs that affect high pressure neurological syndrome.
Br J Pharmacol
March 1994
Department of Biomedical Sciences, Marischal College, University of Aberdeen.
1. Previous studies have suggested that a series of drugs modelled on part of the strychnine molecule interfere with the development of high pressure neurological syndrome (HPNS) and it was presumed that this effect was via an action on inhibitory glycinergic transmission. We have now used the rat hippocampal slice preparation to examine the possibility that some of these drugs might instead have an action at the strychnine-insensitive (SI) glycine binding site associated with the NMDA receptor.
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