Adult-born granule cells (abGCs) exhibit a transient period of elevated synaptic plasticity that plays an important role in hippocampal function. Various mechanisms have been implicated in this critical period for enhanced plasticity, including minimal GABAergic inhibition and high intrinsic excitability conferred by T-type Ca²⁺ channels. Here we assess the contribution of synaptic inhibition and intrinsic excitability to long-term potentiation (LTP) in abGCs of adult male and female mice using perforated patch recordings. We show that the timing of critical period plasticity is unaffected by intact GABAergic inhibition such that 4–6-week-old abGCs exhibit LTP that is absent by 8 weeks. Blocking GABA_A receptors, or partial blockade of GABA release from PV and nNos-expressing interneurons by a µ-opioid receptor agonist, strongly enhances LTP in 4-week-old GCs, suggesting that minimal inhibition does not underlie critical period plasticity. Instead, the closure of the critical period coincides with a reduction in the contribution of T-type Ca²⁺ channels to intrinsic excitability, and a selective T-type Ca²⁺ channel antagonist prevents LTP in 4-week-old but not mature GCs. Interestingly, whole-cell recordings that facilitate T-type Ca²⁺ channel activity in mature GCs unmasks LTP (with inhibition intact) that is also sensitive to a T-type Ca²⁺ channel antagonist, suggesting T-type channel activity in mature GCs is suppressed by native intracellular signaling. Together these results show that abGCs use T-type Ca²⁺ channels to overcome inhibition, providing new insight into how high intrinsic excitability provides young abGCs a competitive advantage for experience-dependent synaptic plasticity.

成年颗粒细胞（abGC）表现出短暂的突触可塑性升高，这在海马功能中发挥着重要作用。在这个增强可塑性的关键时期涉及多种机制，包括最小的 GABA 能抑制和 T 型 Ca ²⁺通道赋予的高内在兴奋性。在这里，我们使用穿孔贴片记录评估了突触抑制和内在兴奋性对成年雄性和雌性小鼠 abGC 长时程增强 (LTP) 的贡献。我们发现，关键期可塑性的时间不受完整 GABA 能抑制的影响，因此 4-6 周龄的 abGC 表现出 8 周时消失的 LTP。阻断 GABA _A受体，或通过 µ-阿片受体激动剂部分阻断 PV 和表达 nNos 的中间神经元释放 GABA，可强烈增强 4 周龄 GC 中的 LTP，表明最小的抑制并不构成关键期可塑性的基础。相反，关键期的结束与 T 型 Ca ²⁺通道对内在兴奋性的贡献减少同时发生，并且选择性 T 型 Ca ²⁺通道拮抗剂可预防 4 周龄但不成熟的 GC 中的 LTP 。有趣的是，促进成熟GC中T型Ca ²⁺通道活性的全细胞记录揭示了对T型Ca ²⁺通道拮抗剂也敏感的LTP（抑制完整），表明成熟GC中存在T型通道活性受到天然细胞内信号传导的抑制。这些结果共同表明，abGC 使用 T 型 Ca ²⁺通道来克服抑制，这为了解高内在兴奋性如何为年轻的 abGC 提供依赖于经验的突触可塑性的竞争优势提供了新的见解。