Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2008-5-27
pubmed:abstractText
Activity in descending systems from the brainstem modulates nociceptive transmission through the dorsal horn. Intrathecal injection of the neurotoxin saporin conjugated to SP (SP-SAP) into the lumbar spinal cord results in the selective ablation of NK(1) receptor expressing (NK(1)+ve) neurones in the superficial dorsal horn (lamina I/III). Loss of these NK(1)+ve neurones attenuates excitability of deep dorsal horn neurones due to a disruption of both intrinsic spinal circuits and a spino-bulbo-spinal loop, which activates a descending excitatory drive, mediated through spinal 5HT(3) receptors. Descending inhibitory pathways also modulate spinal activity and hence control the level of nociceptive transmission relayed to higher centres. To ascertain the spinal origins of the major descending noradrenergic inhibitory pathway we studied the effects of a selective alpha2-adrenoceptor antagonist, atipamezole, on neuronal activity in animals pre-treated with SP-SAP. Intrathecal application of atipamezole dose dependently facilitated the mechanically evoked neuronal responses of deep dorsal horn neurones to low intensity von Frey hairs (5-15 g) and noxious thermal (45-50 degrees C) evoked responses in SAP control animals indicating a physiological alpha2-adrenoceptor control. This facilitatory effect of atipamezole was lost in the SP-SAP treated group. These data suggest that activity within noradrenergic pathways have a dependence on dorsal horn NK(1)+ve cells. Further, noradrenergic descending inhibition may in part be driven by lamina I/III (NK(1)+ve) cells, and mediated via spinal alpha2-adrenoceptor activation. Since the same neuronal population drives descending facilitation and inhibition, the reduced excitability of lamina V/VI WDR neurones seen after loss of these NK(1)+ve neurones indicates a dominant role of descending facilitation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0028-3908
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1208-14
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:18462764-Adrenergic alpha-2 Receptor Antagonists, pubmed-meshheading:18462764-Adrenergic alpha-Antagonists, pubmed-meshheading:18462764-Animals, pubmed-meshheading:18462764-Antineoplastic Agents, Phytogenic, pubmed-meshheading:18462764-Electric Stimulation, pubmed-meshheading:18462764-Electrophysiology, pubmed-meshheading:18462764-Evoked Potentials, pubmed-meshheading:18462764-Hot Temperature, pubmed-meshheading:18462764-Imidazoles, pubmed-meshheading:18462764-Immunohistochemistry, pubmed-meshheading:18462764-Nerve Fibers, Myelinated, pubmed-meshheading:18462764-Nerve Fibers, Unmyelinated, pubmed-meshheading:18462764-Neurons, pubmed-meshheading:18462764-Physical Stimulation, pubmed-meshheading:18462764-Posterior Horn Cells, pubmed-meshheading:18462764-Rats, pubmed-meshheading:18462764-Rats, Sprague-Dawley, pubmed-meshheading:18462764-Receptors, Adrenergic, alpha-2, pubmed-meshheading:18462764-Receptors, Neurokinin-1, pubmed-meshheading:18462764-Ribosome Inactivating Proteins, Type 1, pubmed-meshheading:18462764-Spinal Cord
pubmed:year
2008
pubmed:articleTitle
Selective ablation of dorsal horn NK1 expressing cells reveals a modulation of spinal alpha2-adrenergic inhibition of dorsal horn neurones.
pubmed:affiliation
Department of Pharmacology, University College London, Gower Street, London WC1E 6BT, UK. w.rahman@ucl.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't