Linked Life Data

1359456

Source:http://linkedlifedata.com/resource/pubmed/id/1359456

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1992-12-14
pubmed:abstractText
Peripheral administration of low doses of dopamine agonist apomorphine induces a strong and short-latency inhibition of dopamine neurons in the substantia nigra, presumably via the activation of somatodendritic autoreceptors. We studied the site of action of apomorphine in anesthetized rats using volume-controlled pressure microejection combined with single unit recordings. Microapplication of apomorphine in the immediate vicinity of nigral dopamine neurons did not mimic the effect of intravenous administration of apomorphine (50 micrograms/kg), regardless of the concentration or volume used (10(-10)-10(-2) M, 10-100 nl). In contrast, the inhibition produced by systemic apomorphine was mimicked by drug application at a site 300 microns lateral and 600 microns ventral from the recording site in the zona reticulata of the substantia nigra, a region rich in dendrites of dopamine neurons. The inhibition induced by such a distant application of apomorphine could be reversed by systemic injection of D2, but not D1, receptor antagonists. Non-dopaminergic substances such as GABA, bicuculline or lidocaine were more effective when ejected close to rather than distant from the recording site, in a manner opposite to that of apomorphine. Similar to apomorphine, dopamine and D2 receptor agonists were more potent when intranigral applications were made at sites distant from, rather than close to, the recorded dopamine cells. Ejection of D2 antagonists in the substantia nigra zona reticulata attenuated the inhibitory effect of subsequent systemic apomorphine. Our results, together with other previous studies on the location of D2 receptors on dopamine neurons, suggest that peripheral administration of low doses of apomorphine inhibits nigral dopamine neurons by acting at D2 receptors located on the dendrites of these neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
879-91
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:1359456-Animals, pubmed-meshheading:1359456-Apomorphine, pubmed-meshheading:1359456-Benzazepines, pubmed-meshheading:1359456-Bicuculline, pubmed-meshheading:1359456-Dopamine, pubmed-meshheading:1359456-Dopamine Agents, pubmed-meshheading:1359456-Dose-Response Relationship, Drug, pubmed-meshheading:1359456-Ergolines, pubmed-meshheading:1359456-Evoked Potentials, pubmed-meshheading:1359456-Haloperidol, pubmed-meshheading:1359456-Injections, Intravenous, pubmed-meshheading:1359456-Lidocaine, pubmed-meshheading:1359456-Male, pubmed-meshheading:1359456-Microinjections, pubmed-meshheading:1359456-Neurons, pubmed-meshheading:1359456-Phenethylamines, pubmed-meshheading:1359456-Quinpirole, pubmed-meshheading:1359456-Rats, pubmed-meshheading:1359456-Rats, Wistar, pubmed-meshheading:1359456-Substantia Nigra, pubmed-meshheading:1359456-gamma-Aminobutyric Acid
pubmed:year
1992
pubmed:articleTitle
Inhibition of nigral dopamine neurons by systemic and local apomorphine: possible contribution of dendritic autoreceptors.
pubmed:affiliation
INSERM U171, CNRS URA1195, Centre Hospitalier Lyon-Sud, Pierre Bénite, France.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't