Channels ( IF 3.3 ) Pub Date : 2020-08-15 Preethy S. Sridharan, Yuan Lu, Richard C Rice, Andrew A. Pieper, Anjali M. Rajadhyaksha
ABSTRACT
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.
中文翻译:
Cav1.2通道的丧失会损害海马theta爆发刺激引起的长期增强作用
摘要
CACNA1 C编码L型Ca 2+通道(LTCC)的Ca v 1.2同工型,是神经精神病和神经退行性疾病中的重要风险基因。LTCC,尤其是Ca v 1.2在转录依赖性晚期长期增强(LTP)中的作用早已为人所知。在这里,我们报告说,消除谷氨酸能神经元中的Ca v 1.2通道也会损害theta爆发刺激(TBS)诱导的海马LTP,这是转录独立的并且依赖于N-甲基D-天冬氨酸受体(NMDARs)和局部突触中的蛋白质合成。我们扩大了Ca v的既定作用LTP中的1.2通道可拓宽对突触可塑性的理解,并确定新的细胞表型,以探索认知功能障碍的治疗策略。