Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-6-30
pubmed:abstractText
Depolarization responses to tachykinin receptor agonists were recorded extracellularly from lumbar ventral roots of spinal cord isolated from neonatal rats (one to eight days post partum). All spinal cords were hemisected in the sagittal plane. In addition, in some hemisected cords, the dorsal horns were removed by means of a further cut, perpendicular to the first. In both hemisected and quadrisected spinal cords, reproducible depolarization responses were induced by low concentrations of the neurokinin-1-selective agonist substance P methylester (10 nM-1 microM) or of the neurokinin-3-selective agonist senktide (3-300 nM). On both types of preparation, responses to substance P methylester (1 microM) or senktide (300 nM) were of comparable size. The amplitude of the response to senktide (300 nM) was reduced by at least 88% in spinal cord preparations exposed to tetrodotoxin (0.5 microM) or to physiological medium containing magnesium chloride (20 mM). In contrast, under either of these conditions, concentration-response curves to substance P methylester were shifted rightward by 2.8-8.5-fold, with little effect on the maximum response. Responses to senktide were blocked selectively by the N-methyl-D-aspartate antagonist 3-[(+-)-2-carboxypiperazine-4-yl]propyl-1-phosphonic acid (100 microM); the antagonist had little effect on substance P methylester-induced depolarization (mean concentration ratio 2.0). These results suggest that in the neonatal rat spinal cord, application of exogenous tachykinin agonists can induce ventral root depolarization by activation of neurokinin-1 and/or neurokinin-3 receptors. The response to stimulation of neurokinin-1 receptors has a major component likely to be due to a direct action at motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/3-(2-carboxypiperazin-4-yl)propyl-1-..., http://linkedlifedata.com/resource/pubmed/chemical/Magnesium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/Neuromuscular Depolarizing Agents, http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments, http://linkedlifedata.com/resource/pubmed/chemical/Piperazines, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurotransmitter, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tachykinin, http://linkedlifedata.com/resource/pubmed/chemical/Substance P, http://linkedlifedata.com/resource/pubmed/chemical/Tachykinins, http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin, http://linkedlifedata.com/resource/pubmed/chemical/senktide, http://linkedlifedata.com/resource/pubmed/chemical/substance P, methyl ester-
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
217-23
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Characterization of tachykinin-induced ventral root depolarization in the neonatal rat isolated spinal cord.
pubmed:affiliation
Department of Neuropharmacology, Glaxo Group Research Ltd, Ware, Hertfordshire, U.K.
pubmed:publicationType
Journal Article, In Vitro