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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1986-6-6
pubmed:abstractText
The effect of lesioning noradrenergic pathways on the benzodiazepine receptor has been studied using a novel neurotoxic agent, N(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) which has better selectivity than the classical 6-hydroxydopamine (6-OHDA) towards noradrenergic neurones, and which has the added advantage of being injected systemically rather than intracerebrally. Three different radioligands were used: an agonist, [3H]flunitrazepam, an antagonist, [3H]Ro 15-1788, and a partial agonist [3H]RU 43028. Binding was measured using membrane homogenates from the cortex and hippocampus of the rat, two regions of the brain which receive an extensive noradrenergic innervation. In contrast to previous reports of a decrease in the binding of [3H]flunitrazepam following lesioning with 6-OHDA, no significant change was observed in either the affinity (KD) or the number of sites (Bmax) of any one of these ligands after lesioning with DSP4. While the reasons for this discrepancy are not clear, these results do not confirm that destruction of noradrenergic afferents to the cortex or hippocampus leads to any modification of the benzodiazepine receptor as demonstrated by ligand binding.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0028-3908
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
283-6
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Lesion of noradrenergic neurones with DSP4 does not modify benzodiazepine receptor binding in cortex and hippocampus of rat.
pubmed:publicationType
Journal Article