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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2002-10-30
pubmed:abstractText
High threshold noxious heat-activated currents and vanilloid receptor-like protein-1 expression were studied in rat cultured primary sensory neurons to find out the molecule(s) responsible for high threshold noxious heat-sensitivity. The average temperature threshold and amplitude of high threshold noxious heat-activated currents were 51.6 +/- 0.13 degrees C and -2.0 +/- 0.1nA (at a holding potential of -60 mV), respectively. The current-voltage relationship of high threshold noxious heat-activated currents was linear at positive membrane potentials, while it showed a weak inward rectification at negative membrane potentials. The average reversal potential measured in control intracellular and extracellular solutions was 4.5 +/- 0.9 mV (n = 6). Ionic substitutions revealed that the high threshold noxious heat-activated current is a nonselective cationic current with calculated ionic permeabilities of Cs+ : Na+ : Ca2+ (1 : 1.3 : 4.5). Consecutive stimuli reduced the heat threshold from 52.2 +/- 1 to 48.4 +/- 1.4 degrees C and then to 44 +/- 0.7 degrees C (n = 3). High threshold noxious heat-activated currents could dose-dependently and reversibly be reduced by ruthenium red (100 nm-10 micro m) but not by capsazepine (10 micro m). The average longest diameter of high threshold noxious heat-sensitive neurons was 31.48 +/- 0.5 micro m (A = approximately 778 micro m2; n = 77). Twenty-three percent of the total neuronal population expressed vanilloid receptor-like protein-1. The average area of the vanilloid receptor-like protein-1-immunopositive cells was 1,696 +/- 65.3 micro m2 (d = approximately 46 micro m). Vanilloid receptor-like protein-1-expressing neurons did not express the vanilloid receptor 1. Comparison of our data with results obtained in vanilloid receptor-like protein-1-expressing non-neuronal cells and previous immunohistochemical findings suggests that high threshold noxious heat-activated currents are produced by vanilloid receptor-like protein-1 and that high threshold heat-sensitive dorsal root ganglion neurons are the perikarya of type I noxious heat-sensitive fibers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1483-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:12405961-Afferent Pathways, pubmed-meshheading:12405961-Animals, pubmed-meshheading:12405961-Calcium Signaling, pubmed-meshheading:12405961-Capsaicin, pubmed-meshheading:12405961-Cell Size, pubmed-meshheading:12405961-Cells, Cultured, pubmed-meshheading:12405961-Dose-Response Relationship, Drug, pubmed-meshheading:12405961-Ganglia, Spinal, pubmed-meshheading:12405961-Hot Temperature, pubmed-meshheading:12405961-Immunohistochemistry, pubmed-meshheading:12405961-Male, pubmed-meshheading:12405961-Membrane Potentials, pubmed-meshheading:12405961-Neurons, Afferent, pubmed-meshheading:12405961-Nociceptors, pubmed-meshheading:12405961-Pain, pubmed-meshheading:12405961-Pain Threshold, pubmed-meshheading:12405961-Rats, pubmed-meshheading:12405961-Rats, Sprague-Dawley, pubmed-meshheading:12405961-Receptors, Drug, pubmed-meshheading:12405961-Ruthenium Red, pubmed-meshheading:12405961-Synaptic Transmission, pubmed-meshheading:12405961-TRPV Cation Channels, pubmed-meshheading:12405961-Thermosensing
pubmed:year
2002
pubmed:articleTitle
The putative role of vanilloid receptor-like protein-1 in mediating high threshold noxious heat-sensitivity in rat cultured primary sensory neurons.
pubmed:affiliation
Department of Anaesthetics and Intensive Care, Imperial College, Faculty of Medicine, Chelsea and Westminster Hospital, 369 Fulham Road, London, SW10 9NH, UK.
pubmed:publicationType
Journal Article