Onozuka M, Furuichi H, Fukami Y
Department of Anatomy, Gifu University School of Medicine, Japan.
Neurosci Lett. 1991 Feb 25;123(2):257-60. doi: 10.1016/0304-3940(91)90945-p.
The role of cAMP-dependent protein phosphorylation in the pentylenetetrazole (PTZ)-induced bursting activity was examined in snail neurons, using the voltage clamp method in combination with the pressure injection technique. The cAMP-dependent protein kinase inhibitors, protein kinase inhibitor isolated from rabbit muscle and isoquinolinesulfonamide, inhibited the PTZ-induced negative slope resistance (NSR) in the steady state I-V curve. These inhibitors also suppressed the action of PTZ on the delayed outward potassium current (IKD). This suppression was transiently abolished by intracellular injection of the catalytic subunit of cAMP-dependent protein kinase. These findings suggest that cAMP-dependent protein phosphorylation may be involved in both the development of the NSR and a reduction of the IKD by PTZ, leading to depolarizing phase of a bursting cycle.
利用电压钳技术结合压力注射技术,在蜗牛神经元中研究了环磷酸腺苷(cAMP)依赖性蛋白磷酸化在戊四氮(PTZ)诱导的爆发活动中的作用。cAMP依赖性蛋白激酶抑制剂,即从兔肌肉中分离得到的蛋白激酶抑制剂和异喹啉磺酰胺,在稳态电流-电压(I-V)曲线中抑制了PTZ诱导的负斜率电阻(NSR)。这些抑制剂还抑制了PTZ对延迟外向钾电流(IKD)的作用。通过细胞内注射cAMP依赖性蛋白激酶的催化亚基,这种抑制作用被短暂消除。这些发现表明,cAMP依赖性蛋白磷酸化可能参与了NSR的形成以及PTZ对IKD的降低作用,从而导致爆发周期的去极化阶段。