Ikeuchi Y, Nishizaki T
Department of Physiology, Kobe University School of Medicine, Japan.
Neurosci Lett. 1995 May 5;190(2):89-92. doi: 10.1016/0304-3940(95)11508-t.
The effect of ATP on cultured striatal neurons was examined by whole cell voltage clamp recordings. ATP produced outwardly rectifying currents that reversed near the expected equilibrium potential for the potassium ion and the currents were blocked by intracellular Cs+. Purinergic receptor agonists such as ADP, AMP adenosine, and 2-methylthio ATP (2-MeSATP) also evoked similar outward currents. The order of their potencies was ATP >> 2-MeSATP > or = ADP > adenosine > AMP, corresponding to a P2 purinergic receptor. ATP-evoked currents were blocked by a specific protein kinase C (PKC) inhibitor, GF109203X. In addition, the intracellular perfusion of a G-protein inactivator, GDP beta S abolished ATP-induced currents, whereas pertussis toxin (PTX) had no effect on the currents. These results suggest that ATP activates a potassium channel in striatal neurons, which is regulated by protein kinase C (PKC) activation through a P2 purinergic receptor linked to PTX-insensitive G protein.
通过全细胞膜片钳记录来检测ATP对培养的纹状体神经元的作用。ATP产生外向整流电流,该电流在钾离子预期的平衡电位附近反转,并且该电流被细胞内的Cs⁺阻断。嘌呤能受体激动剂,如ADP、AMP、腺苷和2-甲硫基ATP(2-MeSATP)也诱发类似的外向电流。它们的效力顺序为ATP >> 2-MeSATP ≥ ADP > 腺苷 > AMP,对应于P2嘌呤能受体。ATP诱发的电流被一种特异性蛋白激酶C(PKC)抑制剂GF109203X阻断。此外,细胞内灌注G蛋白失活剂GDPβS可消除ATP诱导的电流,而百日咳毒素(PTX)对该电流无影响。这些结果表明,ATP激活纹状体神经元中的钾通道,该通道通过与对PTX不敏感的G蛋白相连的P2嘌呤能受体由蛋白激酶C(PKC)激活来调节。