Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-7-3
pubmed:abstractText
Activation of spinal N-methyl-D-aspartate (NMDA) receptors and then the nitric oxide and the arachidonic acid pathways is important in pain transmission. This study assessed the effects of the NMDA receptor channel blocker ketamine, the nitric oxide synthase inhibitor L-NAME, and the cyclooxygenase inhibitor ketoprofen in nociceptive transmission using an in vitro neonatal rat spinal cord preparation. Supramaximal electrical stimulation of the dorsal root evoked the A-fibre- and C-fibre-mediated high intensity excitatory postsynaptic potential (EPSP) in the ipsilateral ventral root. Low intensity stimulation evoked the A-fibre-mediated monosynaptic compound action potential (MSR) superimposed on the low intensity EPSP. Both the low intensity EPSP and the high intensity EPSP contain NMDA-receptor-mediated components. Only ketamine and ketoprofen depressed the synaptic responses. Ketamine depressed all three spinal reflexes with IC(50) values (with 95% CI) of 10.80 microM (5.97 to 19.54 microM) for the MSR, 8.29 microM (4.53 to 14.17 microM) for the low intensity EPSP, and 5.35 microM (3.05 to 9.40 microM) for the high intensity EPSP. Ketoprofen depressed the low intensity EPSP and the high intensity EPSP only; IC(50) values (with 95% CI) were 354.5 microM (217.5 to 576.8 microM) and 302.7 microM (174.0 to 526.7 microM), respectively. Reflexes recovered after drug washout. These data demonstrated that ketamine and ketoprofen, but not L-NAME, depressed NMDA-mediated nociceptive transmission in spinal cord preparations from neonatal rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
1094
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
57-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16716267-Afferent Pathways, pubmed-meshheading:16716267-Animals, pubmed-meshheading:16716267-Animals, Newborn, pubmed-meshheading:16716267-Cyclooxygenase Inhibitors, pubmed-meshheading:16716267-Dose-Response Relationship, Drug, pubmed-meshheading:16716267-Down-Regulation, pubmed-meshheading:16716267-Enzyme Inhibitors, pubmed-meshheading:16716267-Excitatory Amino Acid Antagonists, pubmed-meshheading:16716267-Excitatory Postsynaptic Potentials, pubmed-meshheading:16716267-Female, pubmed-meshheading:16716267-Ketamine, pubmed-meshheading:16716267-Ketoprofen, pubmed-meshheading:16716267-Male, pubmed-meshheading:16716267-NG-Nitroarginine Methyl Ester, pubmed-meshheading:16716267-Nitric Oxide Synthase, pubmed-meshheading:16716267-Organ Culture Techniques, pubmed-meshheading:16716267-Pain, pubmed-meshheading:16716267-Pain Threshold, pubmed-meshheading:16716267-Rats, pubmed-meshheading:16716267-Rats, Sprague-Dawley, pubmed-meshheading:16716267-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:16716267-Reflex, pubmed-meshheading:16716267-Spinal Cord, pubmed-meshheading:16716267-Spinal Nerve Roots, pubmed-meshheading:16716267-Synaptic Transmission
pubmed:year
2006
pubmed:articleTitle
Depression of NMDA-receptor-mediated segmental transmission by ketamine and ketoprofen, but not L-NAME, on the in vitro neonatal rat spinal cord preparation.
pubmed:affiliation
IVABS, Massey University, Private Bag 11222, Palmerston North, New Zealand. madrigal@servidor.unam.mx
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't