D1 receptors physically interact with N-type calcium channels to regulate channel distribution and dendritic calcium entry

被引：90

作者：

Kisilevsky, Alexandra E. ^{[1
]}

Mulligan, Sean J. ^{[2
]}

Altier, Christophe ^{[1
]}

Iftinca, Mircea C. ^{[1
]}

Varela, Diego ^{[1
]}

Tai, Chao ^{[3
]}

Chen, Lina ^{[1
]}

Hameed, Shahid ^{[1
]}

Hamid, Jawed ^{[1
]}

MacVicar, Brian A. ^{[3
]}

Zamponi, Gerald W. ^{[1
]}

机构：

[1] Univ Calgary, Hotchkiss Brain Inst, Dept Physiol & Biophys, Calgary, AB T2N 4N1, Canada

[2] Univ Saskatchewan, Dept Physiol, Saskatoon, SK S7N 5E5, Canada

[3] Univ British Columbia, Brain Res Ctr, Vancouver, BC V6T 1Z3, Canada

来源：

NEURON | 2008年 / 58卷 / 04期

关键词：

D O I：

10.1016/j.neuron.2008.03.002

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Dopamine signaling through D1 receptors in the prefrontal cortex (PFC) plays a critical role in the maintenance of higher cognitive functions, such as working memory. At the cellular level, these functions are predicated to involve alterations in neuronal calcium levels. The dendrites of PFC neurons express D1 receptors and N-type calcium channels, yet little information exists regarding their coupling. Here, we show that D1 receptors potently inhibit N-type channels in dendrites of rat PFC neurons. Using coimmunoprecipitation, we demonstrate the existence of a D1 receptor-N-type channel signaling complex in this region, and we provide evidence for a direct receptor-channel interaction. Finally, we demonstrate the importance of this complex to receptor-channel colocalization in heterologous systems and in PFC neurons. Our data indicate that the N-type calcium channel is an important physiological target of D1 receptors and reveal a mechanism for D1 receptor-mediated regulation of cognitive function in the PFC.

引用

页码：557 / 570

页数：14

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