Network oscillations at γ frequency band (30–80 Hz), generated by the interaction between inhibitory interneurons and excitatory neurons, have been proposed to be associated with higher brain functions such as learning and memory. Dopamine (DA), one of the major CNS transmitters, modulates hippocampal γ oscillations but the intracellular mechanisms involved remain elusive. In this study, we recorded kainate-induced γ oscillations in the CA3 area of rat hippocampal slices, and found that DA strongly enhanced γ power, which was largely blocked by dopamine receptor 1 (DR1) antagonist SCH23390, receptor tyrosine kinase (RTK) inhibitor UNC569 and ERK inhibitor U0126, partially blocked by D2/3R antagonist raclopride, PKA inhibitor H89 and PI3K inhibitor wortmannin, but not affected by AKT inhibitor TCBN or NMDAR antagonist D-AP5. Our results indicate that DA-mediated γ enhancement is involved in the activation of signaling pathway of DR1/2-RTK-ERK. Our data demonstrate a strong, rapid modulation of DA on hippocampal γ oscillations and provide a new insight into cellular mechanisms of DA-mediated γ oscillations.

由抑制性中间神经元和兴奋性神经元之间的相互作用产生的 γ 频带（30-80 Hz）的网络振荡被认为与学习和记忆等高级大脑功能有关。多巴胺 (DA) 是主要的 CNS 递质之一，可调节海马 γ 振荡，但所涉及的细胞内机制仍然难以捉摸。在这项研究中，我们记录了大鼠海马切片 CA3 区海人酸诱导的 γ 振荡，发现 DA 强烈增强 γ 功率，这在很大程度上被多巴胺受体 1 (DR1) 拮抗剂 SCH23390、受体酪氨酸激酶 (RTK) 抑制剂所阻断UNC569 和 ERK 抑制剂 U0126，被 D2/3R 拮抗剂 raclopride、PKA 抑制剂 H89 和 PI3K 抑制剂渥曼青霉素部分阻断，但不受 AKT 抑制剂 TCBN 或 NMDAR 拮抗剂 D-AP5 的影响。我们的结果表明 DA 介导的 γ 增强参与了 DR1/2-RTK-ERK 信号通路的激活。我们的数据证明了 DA 对海马 γ 振荡的强烈、快速调制，并提供了对 DA 介导的 γ 振荡的细胞机制的新见解。