Schröder H, Reymann K G, Matthies H
Institute of Pharmacology and Toxicology, Medical Academy Magdeburg, GDR.
Biomed Biochim Acta. 1989;48(7):425-9.
Slices of rat hippocampus were labelled with [14C]dopamine, superfused continuously with oxygenated Krebs-Henseleit solution and stimulated with a potassium pulse (48 mM K+, 5 min.). 4-beta-phorbol-12,13-dibutyrate (PDB), an activator of protein kinase C (PKC), enhanced the potassium-evoked overflow of 14C. This effect was blocked by prior application of polymyxin B, a relatively selective inhibitor of PKC. In contrast, the PKC-inactive 4-alpha-phorbol-12,13-didecanoate (PDD) had no influence on the evoked transmitter overflow. The results suggest that PKC may also be involved in the regulation of hippocampal DA release. A possible link between PKC activation and DA release to processes of synaptic long-term potentiation is discussed.
将大鼠海马体切片用[14C]多巴胺标记,持续用含氧的克雷布斯 - 亨泽莱特溶液进行灌流,并用电刺激(48 mM K +,5分钟)。蛋白激酶C(PKC)的激活剂4-β-佛波醇-12,13-二丁酸酯(PDB)增强了钾诱发的14C溢出。这种作用被预先应用的多粘菌素B阻断,多粘菌素B是一种相对选择性的PKC抑制剂。相比之下,PKC无活性的4-α-佛波醇-12,13-二癸酸酯(PDD)对诱发的递质溢出没有影响。结果表明PKC可能也参与海马体多巴胺释放的调节。讨论了PKC激活与多巴胺释放到突触长期增强过程之间的可能联系。