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- Title
The Ubiquitin—Proteasome System Is Necessary for Long-Term Synaptic Depression in Aplysia.
- Authors
Fioravante, Diasinou; Rong-Yu Liu; Byrne, John H.
- Abstract
The neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFa) can induce transcription-dependent long-term synaptic depression (LTD) in Aplysia sensorimotor synapses. We investigated the role of the ubiquitin-proteasome system and the regulation of one of its components, ubiquitin C-terminal hydrolase (ap-uch), in LTD. LTD was sensitive to presynaptic inhibition of the proteasome and was associated with upregulation of ap-uch mRNA and protein. This upregulation appeared to be mediated by CREB2, which is generally regarded as a transcription repressor. Binding of CREB2 to the promoter region of ap-uch was accompanied by histone hyperacetylation, suggesting that CREB2 cannot only inhibit but also promote gene expression. CREB2 was phosphorylated after FMRFa, and blocking phospho-CREB2 blocked LTD. In addition to changes in the expression of ap-uch, the synaptic vesicle-associated protein synapsin was downregulated inLTDin a proteasome-dependent manner. These results suggest that proteasome-mediated protein degradation is engaged in LTD and that CREB2 may act as a transcription activator under certain conditions.
- Subjects
NEURAL transmission; APLYSIA; SYNAPSES; GENETIC regulation; PROTEINS; UBIQUITIN
- Publication
Journal of Neuroscience, 2008, Vol 28, Issue 41, p10245
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.2139-08.2008