Dopamine receptor regulation of Ca2+ levels in individual isolated nerve terminals from rat striatum: comparison of presynaptic D1-like and D2-like receptors.
Dopamine receptor regulation of Ca2+ levels in individual isolated nerve terminals from rat striatum: comparison of presynaptic D1-like and D2-like receptors.
复制标题
多巴胺受体对大鼠纹状体单个分离神经末梢 Ca2 水平的调节:突触前 D1 样和 D2 样受体的比较。
DOI:
10.1111/j.1471-4159.2006.03901.x
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发表时间:
2006
期刊:
影响因子:
--
通讯作者:
Nichols,RobertA
中科院分区:
文献类型:
--
作者:
Wu,Jianlin;Dougherty,JohnJ;Nichols,RobertA
We have directly observed the effects of activating presynaptic D1‐like and D2‐like dopamine receptors on Ca2+levels in isolated nerve terminals (synaptosomes) from rat striatum. R‐(+)‐SKF81297, a selective D1‐like receptor agonist, and (–)‐quinpirole, a selective D2‐like receptor agonist, induced increases in Ca2+levels in different subsets of individual striatal synaptosomes. The SKF81297‐ and quinpirole‐induced effects were blocked by R‐(+)‐SCH23390, a D1‐like receptor antagonist, and (–)‐sulpiride, a D2‐like receptor antagonist, respectively. SKF81297‐ or quinpirole‐induced Ca2+increases were inhibited following blockade of voltage‐gated calcium channels or sodium channels. In a larger subset of synaptosomes, quinpirole decreased baseline Ca2+. Quinpirole also inhibited veratridine‐induced increases in intrasynaptosomal Ca2+level. Immunostaining confirmed the presynaptic expression of D1, D5, D2and D3receptors, but not D4receptors. The array of neurotransmitter phenotypes of the striatal nerve endings expressing D1, D5, D2or D3varied for each receptor subtype. These results suggest that presynaptic D1‐like and D2‐like receptors induce increases in Ca2+levels in different subsets of nerve terminals via Na+channel‐mediated membrane depolarization, which, in turn, induces the opening of voltage‐gated calcium channels. D2‐like receptors also reduce nerve terminal Ca2+in a different but larger subset of synaptosomes, consistent with the predominant presynaptic action of dopamine in the striatum being inhibitory.