Loss of Cav1.2 channels impairs hippocampal theta burst stimulation-induced long-term potentiation.

Loss of Cav1.2 channels impairs hippocampal theta burst stimulation-induced long-term potentiation.
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DOI:
10.1080/19336950.2020.1807851
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发表时间:
2020-12
期刊:
Channels (Austin, Tex.)
影响因子:
--
通讯作者:
Rajadhyaksha AM
Rajadhyaksha AM
中科院分区:
其他
文献类型:
--
作者:
Sridharan PS;Lu Y;Rice RC;Pieper AA;Rajadhyaksha AM

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CACNA 1 C编码L型Ca 2+通道(LTCC)的Cav1.2亚型,是神经精神和神经退行性疾病的主要风险基因。LTCCs,特别是Cav1.2,在转录依赖的晚期长时程增强(LTP)中的作用早已为人们所知。在这里,我们报告说,消除Cav1.2通道在海马神经元也损害θ爆发刺激(TBS)诱导的LTP在海马,已知是转录独立和依赖于N-甲基D-天冬氨酸受体(NMDARs)和当地的蛋白质合成在突触。我们扩大了Cav1.2通道在LTP中的既定作用,拓宽了对突触可塑性的理解,并确定了一种新的细胞表型,用于探索认知功能障碍的治疗策略。
CACNA1 C, which codes for the Cav1.2 isoform of L-type Ca2+ channels (LTCCs), is a prominent risk gene in neuropsychiatric and neurodegenerative conditions. A role forLTCCs, and Cav1.2 in particular, in transcription-dependent late long-term potentiation (LTP) has long been known. Here, we report that elimination of Cav1.2 channels in glutamatergic neurons also impairs theta burst stimulation (TBS)-induced LTP in the hippocampus, known to be transcription-independent and dependent on N-methyl D-aspartate receptors (NMDARs) and local protein synthesis at synapses. Our expansion of the established role of Cav1.2channels in LTP broadens understanding of synaptic plasticity and identifies a new cellular phenotype for exploring treatment strategies for cognitive dysfunction.
DOI: 10.1038/nn.3307
发表时间: 2013-02
影响因子: 25
作者:
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