Kim Yonjung, Park Myoung Kyu, Chung Sungkwon
Department of Physiology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Jangan-ku, Suwon 440-746, South Korea.
Biochem Biophys Res Commun. 2008 Sep 5;373(4):665-9. doi: 10.1016/j.bbrc.2008.06.099. Epub 2008 Jul 2.
Dopamine (DA) neurons release DA not only from axon terminals at the striatum, but from their somata and dendrites at the substantia nigra pars compacta (SNc). Released DA may auto-regulate further DA release or modulate non-DA cells. However, the actual mechanism of somatodendritic DA release, especially the Ca(2+) dependency of the process, remains controversial. In this study, we used amperometry to monitor DA release from somata of acutely isolated rat DA neurons. We found that DA neurons spontaneously released DA in the resting state. Removal of extracellular Ca(2+) and application of blockers for voltage-operated Ca(2+) channels (VOCCs) suppressed the frequency of secretion events. Activation of VOCCs by stimulation with K(+)-rich saline increased the frequency of secretion events, which were also sensitive to blockers for L- and T-type Ca(2+) channels. These results suggest that Ca(2+) influx through VOCCs regulates DA release from somata of DA neurons.
多巴胺（DA）神经元不仅从纹状体的轴突终末释放DA，还从黑质致密部（SNc）的胞体和树突释放DA。释放的DA可能会自动调节进一步的DA释放或调节非DA细胞。然而，树突体DA释放的实际机制，尤其是该过程对Ca(2+)的依赖性，仍存在争议。在本研究中，我们使用安培法监测急性分离的大鼠DA神经元胞体释放DA的情况。我们发现DA神经元在静息状态下会自发释放DA。去除细胞外Ca(2+)并应用电压门控Ca(2+)通道（VOCCs）阻滞剂可抑制分泌事件的频率。用富含K(+)的盐水刺激激活VOCCs会增加分泌事件的频率，这些分泌事件对L型和T型Ca(2+)通道阻滞剂也敏感。这些结果表明，通过VOCCs的Ca(2+)内流调节DA神经元胞体释放DA。
