CaMKII inhibitor 1 (CaMK2N1) mRNA is upregulated following LTP induction in hippocampal slices.,SYNAPSE

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CaMKII inhibitor 1 (CaMK2N1) mRNA is upregulated following LTP induction in hippocampal slices.
SYNAPSE ( IF 1.6 ) Pub Date : 2020-04-22 , DOI: 10.1002/syn.22158
Daniela Astudillo ₁ , Daniel Karmelic ₁ , Barbara S Casas ₂ , Nikolai Otmakhov ₃ , Veronica Palma ₂ , Magdalena Sanhueza ₁

Affiliation

CaMK2N1 and CaMK2N2 (also known as CaMKIINα and β) are endogenous inhibitors of calcium/calmodulin‐dependent kinase II (CaMKII), an enzyme critical for memory and long‐term potentiation (LTP), a form of synaptic plasticity thought to underlie learning. CaMK2N1/2 mRNAs are rapidly and differentially upregulated in the hippocampus and amygdala after acquisition or retrieval of fear memory. Moreover, CaMK2N2 protein levels increase after contextual fear conditioning. Therefore, it was proposed that CaMK2N1/2 genes (Camk2n1/2 ) could be immediate‐early genes transcribed promptly (30–60 min) after training. As a first approach to explore a role in synaptic plasticity, we assessed a possible regulation of Camk2n1/2 during the expression phase of LTP in hippocampal CA3–CA1 connections in rat brain slices. Quantitative PCR revealed that Camk2n1 , but not Camk2n2 , is upregulated 60 min after LTP induction by Schaffer collaterals high‐frequency stimulation. We observed a graded, significant positive correlation between the magnitude of LTP and Camk2n1 change in individual slices, suggesting a coordinated regulation of these properties. If mRNA increment actually resulted in the protein upregulation in plasticity‐relevant subcellular locations, CaMK2N1 may be involved in CaMKII fine‐tuning during LTP maintenance or in the regulation of subsequent plasticity events (metaplasticity).

中文翻译：

海马切片中 LTP 诱导后，CaMKII 抑制剂 1 (CaMK2N1) mRNA 上调。

CaMK2N1 和 CaMK2N2（也称为 CaMKIINα 和 β）是钙/钙调蛋白依赖性激酶 II (CaMKII) 的内源性抑制剂，CaMKII 是一种对记忆和长时程增强 (LTP) 至关重要的酶，LTP 是一种被认为是学习基础的突触可塑性形式。在获得或恢复恐惧记忆后，海马和杏仁核中的 CaMK2N1/2 mRNA 迅速且差异性上调。此外，在情境恐惧调节后，CaMK2N2 蛋白水平会增加。因此，有人提出CaMK2N1/2基因（ Camk2n1/2 ）可以是训练后立即（30-60分钟）转录的早期基因。作为探索突触可塑性作用的第一个方法，我们评估了大鼠脑切片海马 CA3-CA1 连接中 LTP 表达阶段Camk2n1/2的可能调节。定量 PCR 显示，在 Schaffer 络脉高频刺激诱导 LTP 60 分钟后， Camk2n1上调，但Camk2n2不上调。我们观察到单个切片中 LTP 和Camk2n1变化幅度之间存在分级的显着正相关性，表明这些特性的协调调节。如果 mRNA 的增加实际上导致可塑性相关亚细胞位置的蛋白质上调，那么 CaMK2N1 可能参与 LTP 维持期间的 CaMKII 微调或随后的可塑性事件（化塑性）的调节。

更新日期：2020-04-22

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