Linked Life Data

10784105

Source:http://linkedlifedata.com/resource/pubmed/id/10784105

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2000-7-27
pubmed:abstractText
The role of calcium in the modulation of spontaneous [3H]acetylcholine ([3H]ACh) efflux through presynaptic D2 dopamine hetero-receptors was investigated in rat striatal synaptosomes. The kinetic studies of [3H]ACh efflux in the presence or absence of Ca2+ were carried out in nonstimulating conditions. When Ca2+ was omitted from the superfusion medium, a notable and significant (P<0.001) decrease of tritium efflux (39%) was obtained. While [3H]ACh efflux was insensitive to tetrodotoxin (TTX) 1 microM, cadmium (10 microM), a nonselective antagonist of calcium channels, significantly reduced the tritium efflux by 24% (P<0.001), while the L-type calcium antagonist, nifedipine, (30 microM) inhibited the tritium efflux by only 10% (P<0.02). 2-(4-Fenylpiperidine)cyclohexanol (vesamicol), an inhibitor of the vesicular [3H]ACh carrier, significantly depressed the spontaneous tritium efflux in the presence of Ca2+ (60%; P<0.001) and in a low-calcium medium (20%; P<0.001). Although 1 microM of 7-hydroxy-N,N-di-n-propyl-2-aminotetraline (7-OH-DPAT) inhibited spontaneous [3H]ACh efflux in the presence of calcium, this dopaminergic agonist did not modify the neurotransmitter release in either the low-Ca2+ medium or in the presence of vesamicol. These results suggest that the spontaneous [3H]ACh efflux is a process involving a Ca2+-dependent component (39%), sensitive to calcium channel-blockers and vesamicol, in rat striatal synaptosomes. In addition, activation of the D2 dopamine hetero-receptor only modulates the calcium-dependent component of spontaneous [3H]ACh efflux.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/7-hydroxy-2-N,N-dipropylaminotetrali..., http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers, http://linkedlifedata.com/resource/pubmed/chemical/Cholinesterase Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Dopamine Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Physostigmine, http://linkedlifedata.com/resource/pubmed/chemical/Piperidines, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Dopamine D2, http://linkedlifedata.com/resource/pubmed/chemical/Tetrahydronaphthalenes, http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin, http://linkedlifedata.com/resource/pubmed/chemical/Tritium, http://linkedlifedata.com/resource/pubmed/chemical/vesamicol
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
854
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
42-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Role of calcium on the modulation of spontaneous acetylcholine efflux by the D2 dopamine receptor subtype in rat striatal synaptosomes.
pubmed:affiliation
Departament de Farmacologia i Terapèutica, Facultat de Medicina, Universitat Autònoma de Barcelona, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't