Abstract:
:EPAC proteins are the guanine nucleotide exchange factors that act as the intracellular receptors for cyclic AMP. Two variants of EPAC genes including EPAC1 and EPAC2 are cloned and are widely expressed throughout the brain. But, their functions in the brain remain unknown. Here, we genetically delete EPAC1 (EPAC1(-/-)), EPAC2 (EPAC2(-/-)), or both EPAC1 and EPAC2 genes (EPAC(-/-)) in the forebrain of mice. We show that EPAC null mutation impairs long-term potentiation (LTP) and that this impairment is paralleled with the severe deficits in spatial learning and social interactions and is mediated in a direct manner by miR-124 transcription and Zif268 translation. Knockdown of miR-124 restores Zif268 and hence reverses all aspects of the EPAC(-/-) phenotypes, whereas expression of miR-124 or knockdown of Zif268 reproduces the effects of EPAC null mutation. Thus, EPAC proteins control miR-124 transcription in the brain for processing spatial learning and social interactions.
journal_name
Neuronjournal_title
Neuronauthors
Yang Y,Shu X,Liu D,Shang Y,Wu Y,Pei L,Xu X,Tian Q,Zhang J,Qian K,Wang YX,Petralia RS,Tu W,Zhu LQ,Wang JZ,Lu Ydoi
10.1016/j.neuron.2012.02.003subject
Has Abstractpub_date
2012-02-23 00:00:00pages
774-88issue
4eissn
0896-6273issn
1097-4199pii
S0896-6273(12)00128-6journal_volume
73pub_type
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