Source:http://linkedlifedata.com/resource/pubmed/id/10198826
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7-8
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pubmed:dateCreated |
1999-7-7
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pubmed:abstractText |
In slices of human neocortex, prelabelled with [3H]-choline, the release of [3H]-acetylcholine reflects the evoked release of endogenous acetylcholine which was elicited by the same electrical stimulation paradigm. [3H]-Acetylcholine release was depressed by the delta-opioid receptor agonist D-Pen2-D-Pen5-enkephalin. When the nerve endings were depolarized by elevating extracellular potassium the evoked [3H]-acetylcholine release was similarly depressed by D-Pen2-D-Pen5-enkephalin in the absence, but not in the presence, of tetrodotoxin which blocks action potential propagation. Therefore, the delta-opioid receptor inhibiting [3H]-acetylcholine release should not be located to cholinergic nerve terminals, but rather to interneurons. The somatostatin2 receptor partial agonist octreotide per se did not influence action potential-evoked [3H]-acetylcholine release, but prevented the inhibition of release of [3H]-acetylcholine by D-Pen2-D-Pen5-enkephalin. Similarly, the delta 1-opioid receptor antagonist 7-benzylidenenaltrexon per se did not influence [3H]-acetylcholine release, but prevented of the inhibition of release by D-Pen2-D-Pen5-enkephalin. From the present findings we conclude: (1) The evoked release of [3H]-acetylcholine from human neocortex slices reflects the release of endogenous acetylcholine. (2) It is inhibited in an indirect manner by opioid receptors of the delta 1-subtype, which (3) are not localized on cholinergic axon terminals but on soma and dendrites of somatostatin-containing interneurons, where they inhibit somatostatin release. (4) These interneurons innervate cholinergic nerve endings in the human neocortex and appear to facilitate acetylcholine release via somatostatin2 receptors.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/7-benzylidenenaltrexone,
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Benzylidene Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, D-Penicillamine (2,5)-,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalins,
http://linkedlifedata.com/resource/pubmed/chemical/Naltrexone,
http://linkedlifedata.com/resource/pubmed/chemical/Narcotic Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Octreotide,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, delta,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin,
http://linkedlifedata.com/resource/pubmed/chemical/naltrindole
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pubmed:status |
MEDLINE
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pubmed:issn |
0736-5748
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
795-802
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10198826-Acetylcholine,
pubmed-meshheading:10198826-Adult,
pubmed-meshheading:10198826-Aged,
pubmed-meshheading:10198826-Aged, 80 and over,
pubmed-meshheading:10198826-Benzylidene Compounds,
pubmed-meshheading:10198826-Electric Stimulation,
pubmed-meshheading:10198826-Enkephalin, D-Penicillamine (2,5)-,
pubmed-meshheading:10198826-Enkephalins,
pubmed-meshheading:10198826-Humans,
pubmed-meshheading:10198826-Interneurons,
pubmed-meshheading:10198826-Middle Aged,
pubmed-meshheading:10198826-Naltrexone,
pubmed-meshheading:10198826-Narcotic Antagonists,
pubmed-meshheading:10198826-Neocortex,
pubmed-meshheading:10198826-Octreotide,
pubmed-meshheading:10198826-Receptors, Opioid, delta,
pubmed-meshheading:10198826-Tetrodotoxin
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pubmed:articleTitle |
delta 1-Opioid receptor-mediated control of acetylcholine (ACh) release in human neocortex slices.
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pubmed:affiliation |
Sektion Klinische Neuropharmakologie, Neurologischen Universitätsklinik, Neurozentrum, Freiburg, Germany. feuer@ukl.uni-freiburg.de
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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