期刊
LEARNING & MEMORY
卷 17, 期 12, 页码 605-611出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/lm.1991910
关键词
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资金
- Deutsche Forschungsgemeinschaft [FR1034-7, SFB 779 TP B4]
- National Institute of Mental Health [R01MH53576, MH57068]
Dopaminergic D1/D5-receptor-mediated processes are important for certain forms of memory as well as for a cellular model of memory, hippocampal long-term potentiation (LTP) in the CA1 region of the hippocampus. D1/D5-receptor function is required for the induction of the protein synthesis-dependent maintenance of CA1-LTP (L-LTP) through activation of the cAMP/PKA-pathway. In earlier studies we had reported a synergistic interaction of D1/D5-receptor function and N-methyl-D-aspartate (NMDA)-receptors for L-LTP. Furthermore, we have found the requirement of the atypical protein kinase C isoform, protein kinase M zeta (PKM zeta) for conventional electrically induced L-LTP, in which PKM zeta has been identified as a LTP-specific plasticity-related protein (PRP) in apical CA1-dendrites. Here, we investigated whether the dopaminergic pathway activates PKM zeta. We found that application of dopamine (DA) evokes a protein synthesis-dependent LTP that requires synergistic NMDA-receptor activation and protein synthesis in apical CA1-dendrites. We identified PKM zeta as a DA-induced PRP, which exerted its action at activated synaptic inputs by processes of synaptic tagging.
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