Bartmann P, Jackisch R, Hertting G, Allgaier C
Pharmakologisches Institut der Universität, Freiburg, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1989 Mar;339(3):302-5. doi: 10.1007/BF00173582.
A possible participation of protein kinase C (PKC) in depolarization-induced release of gamma-aminobutyric acid (GABA) in rabbit caudate nucleus was examined by means of phorbol esters and staurosporine. Slices of caudate nucleus were loaded with [3H]GABA, then superfused and stimulated electrically (3 ms, 5 Hz, 24 mA, 5 V/cm) for 2 min. Aminooxyacetic acid and the uptake inhibitor nipecotic acid were present throughout. The PKC activator 4 beta-phorbol 12,13-dibutyrate (4 beta-PDB) markedly enhanced the evoked [3H]GABA release. In contrast, its biologically inactive isomer, 4 alpha-PDB, did not facilitate transmitter release. Staurosporine, an inhibitor of PKC, diminished [3H]GABA release and counteracted the effects caused by 4 beta-PDB. The above results suggest a participation of PKC in depolarization-induced GABA release in rabbit caudate nucleus. The mechanism underlying the modulation of GABA release by PKC seems to be independent of presynaptic GABA, dopamine and 5-hydroxytryptamine receptors.
通过佛波酯和星形孢菌素研究了蛋白激酶C（PKC）在兔尾状核去极化诱导的γ-氨基丁酸（GABA）释放中的可能作用。将尾状核切片用[3H]GABA装载，然后进行灌流并电刺激（3毫秒，5赫兹，24毫安，5伏/厘米）2分钟。全程存在氨氧基乙酸和摄取抑制剂尼克酸。PKC激活剂4β-佛波醇12,13-二丁酸酯（4β-PDB）显著增强诱发的[3H]GABA释放。相反，其无生物学活性的异构体4α-PDB则不促进递质释放。PKC抑制剂星形孢菌素减少[3H]GABA释放并抵消4β-PDB引起的效应。上述结果表明PKC参与兔尾状核去极化诱导的GABA释放。PKC调节GABA释放的潜在机制似乎独立于突触前GABA、多巴胺和5-羟色胺受体。
