Neuronal network oscillations in the gamma frequency band (30-80 Hz, γ oscillations) are associated with the higher brain functions such as perception, attention, learning and memory. BK channels mediate rapid repolarization and fast afterhyperpolarization in neurons and control neuronal excitability, and potentially control hippocampal γ oscillations. In this study, we examined the effects of modulating BK channels on hippocampal γ oscillations in the absence or presence of Ca²⁺ influx through voltage-gated Ca²⁺ channels (VGCC) or Ca²⁺ –permeable AMPA receptors (CP-AMPAR). We found that blocking BK channels enhanced γ power, without affecting oscillation frequency or regularity, suggesting that BK channel activity suppresses γ oscillations. Blocking either VGCC or CP-AMPAR itself enhanced γ power, and completely occluded the effect of BK channel blockers on γ oscillations, whereas blocking BK channels first could not prevent a further γ power increase upon blockade of either CP-AMPAR or VGCC. We propose that Ca²⁺ influx through VGCC or CP-AMPAR during γ oscillations, cause membrane BK channel activation and regulate hippocampal γ oscillation strength by negative feedback.

伽马频带（30-80 Hz，γ 振荡）中的神经元网络振荡与感知、注意力、学习和记忆等高级大脑功能有关。BK 通道介导神经元中的快速复极化和快速后超极化并控制神经元兴奋性，并可能控制海马 γ 振荡。在本研究中，我们研究了在 Ca ²⁺通过电压门控 Ca ²⁺通道 (VGCC) 或 Ca ²⁺流入的情况下，调节 BK 通道对海马 γ 振荡的影响– 渗透性 AMPA 受体 (CP-AMPAR)。我们发现阻断 BK 通道增强了 γ 功率，而不影响振荡频率或规律性，这表明 BK 通道活动抑制了 γ 振荡。阻断 VGCC 或 CP-AMPAR 本身增强了 γ 功率，并完全阻断了 BK 通道阻断剂对 γ 振荡的影响，而首先阻断 BK 通道不能阻止在 CP-AMPAR 或 VGCC 阻断后进一步增加 γ 功率。我们提出 Ca ²⁺在 γ 振荡期间通过 VGCC 或 CP-AMPAR 流入，导致膜 BK 通道激活并通过负反馈调节海马 γ 振荡强度。