Ault D T, Werling L L
Neuroscience Program, The George Washington University Medical Center, 2300 I St. NW, Washington, DC 20037, USA.
Brain Res. 2000 Sep 22;877(2):354-60. doi: 10.1016/s0006-8993(00)02722-0.
Previous studies in our laboratory using rat brain tissue have shown that neuropeptide Y (NPY) can enhance NMDA- and potassium-stimulated dopamine release from various brain regions and that this enhancement is reversed by sigma (sigma) receptor antagonists. In the current study, we sought to determine whether SH-SY5Y cells are suitable for investigating sigma receptor effects and whether any sigma receptors present are of the subtype responsive to NPY. We compare mechanisms by which the prototypical sigma receptor agonist (+)-pentazocine, and the proposed endogenous sigma receptor ligand NPY regulate potassium-stimulated [(3)H]dopamine release from SH-SY5Y cells. Both (+)-pentazocine and NPY inhibit potassium-stimulated [(3)H]dopamine release. Unlike our studies in rat brain tissue, the effect of NPY on [(3)H]dopamine release is not reversed by sigma receptor antagonists. SH-SY5Y cells appear to be an appropriate model to study the regulation of dopamine release by sigma receptors or by NPY receptors, but this population is not identical to that population identified in brain slices.
我们实验室先前使用大鼠脑组织进行的研究表明，神经肽Y（NPY）可增强NMDA和钾刺激的来自不同脑区的多巴胺释放，且这种增强作用可被σ受体拮抗剂逆转。在当前研究中，我们试图确定SH-SY5Y细胞是否适合用于研究σ受体效应，以及所存在的任何σ受体是否属于对NPY有反应的亚型。我们比较了典型的σ受体激动剂（+）-喷他佐辛和假定的内源性σ受体配体NPY调节钾刺激的SH-SY5Y细胞[³H]多巴胺释放的机制。（+）-喷他佐辛和NPY均抑制钾刺激的[³H]多巴胺释放。与我们在大鼠脑组织中的研究不同，NPY对[³H]多巴胺释放的作用不能被σ受体拮抗剂逆转。SH-SY5Y细胞似乎是研究σ受体或NPY受体对多巴胺释放调节作用的合适模型，但该细胞群体与脑片中鉴定出的细胞群体并不相同。
