| pubmed-article:2167220 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C1517714 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C0013030 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C0205396 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:2167220 | lifeskim:mentions | umls-concept:C1880022 | lld:lifeskim |
| pubmed-article:2167220 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:2167220 | pubmed:dateCreated | 1990-9-21 | lld:pubmed |
| pubmed-article:2167220 | pubmed:abstractText | The effects of dopamine (DA) on voltage-dependent Ca2+ currents were investigated in cultured rat lactotroph cells using the patch clamp recording technique. Each recorded cell was identified by the reverse hemolytic plaque assay. In the whole-cell configuration, two types of Ca2+ currents, L and T, were characterized on the basis of their kinetics, voltage sensitivity, and pharmacology. The L component had a threshold of -25 mV, showed little inactivation during a 150-msec voltage step, and was maximal at +10 mV. Cadmium ions (100 microM) significantly reduced its amplitude (75%). The T component was activated at a membrane potential close to -50 mV, was maximal at -10 mV, and showed a voltage-dependent inactivation between -90 and -30 mV. It was quickly inactivated during a maintained depolarization (time constant, 27 ms at -30 mV) and was strongly reduced (80%) by nickel ions (100 microM). Bath application of DA (10 nM) caused a markedly general depression of inward Ca2+ currents, acting differently on the T- and L-type currents. DA application shifted the voltage-dependence of the L-type current activation toward depolarization values (8 mV) without modifying its time- and voltage-dependent inactivation. In contrast, DA enhanced the inactivation of the T-type current by accelerating its time-dependent inactivation (25% decrease in the time constant of inactivation) and by shifting the voltage-dependence of the T-type current inactivation toward hyperpolarizing values (-63 mV in control vs. -77 mV in the presence of DA). These effects of DA were dose-dependent and involved the activation of a D2 receptor type. They were mimicked by bromocriptine application (10 nM), whereas sulpiride (100 nM) blocked the DA-evoked response. The D1 antagonist SCH 23390 was ineffective up to 100 microM. All of these DA-induced modifications in Ca2+ currents were abolished using a GTP-free pipette solution or after pretreatment of cells with pertussis toxin, suggesting that DA can regulate the function of Ca2+ channels through GTP-binding proteins (G-proteins). Our results show that DA acts simultaneously by reducing both voltage-dependent Ca2+ currents on lactotroph cells. Thus, DA reduces the entry of Ca2+ ions across the surface membrane and thereby influences electrical activity and the cytosolic free Ca2+ concentration involved in both basal and evoked PRL release. | lld:pubmed |
| pubmed-article:2167220 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2167220 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:2167220 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2167220 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:2167220 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:2167220 | pubmed:author | pubmed-author:VincentJ DJD | lld:pubmed |
| pubmed-article:2167220 | pubmed:author | pubmed-author:LegendrePP | lld:pubmed |
| pubmed-article:2167220 | pubmed:author | pubmed-author:LledoP MPM | lld:pubmed |
| pubmed-article:2167220 | pubmed:author | pubmed-author:IsraelJ MJM | lld:pubmed |
| pubmed-article:2167220 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2167220 | pubmed:volume | 127 | lld:pubmed |
| pubmed-article:2167220 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2167220 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2167220 | pubmed:pagination | 990-1001 | lld:pubmed |
| pubmed-article:2167220 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
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| pubmed-article:2167220 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2167220 | pubmed:articleTitle | Dopamine inhibits two characterized voltage-dependent calcium currents in identified rat lactotroph cells. | lld:pubmed |
| pubmed-article:2167220 | pubmed:affiliation | INSERM U.176, 33077 Bordeaux, France. | lld:pubmed |
| pubmed-article:2167220 | pubmed:publicationType | Journal Article | lld:pubmed |
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