title: BDNF facilitates L-LTP maintenance in the absence of protein synthesis through PKMζ.
abstract: Late-phase long term potentiation (L-LTP) is thought to be the cellular basis for long-term memory (LTM). While LTM as well as L-LTP is known to depend on transcription and translation, it is unclear why brain-derived neurotrophic factor (BDNF) could sustain L-LTP when protein synthesis is inhibited. The persistently active protein kinase ζ (PKMζ) is the only molecule implicated in perpetuating L-LTP maintenance. Here, in mouse acute brain slices, we show that inhibition of PKMζ reversed BDNF-dependent form of L-LTP. While BDNF did not alter the steady-state level of PKMζ, BDNF together with the L-LTP inducing theta-burst stimulation (TBS) increased PKMζ level even without protein synthesis. Finally, in the absence of de novo protein synthesis, BDNF maintained TBS-induced PKMζ at a sufficient level. These results suggest that BDNF sustains L-LTP through PKMζ in a protein synthesis-independent manner, revealing an unexpected link between BDNF and PKMζ.
authors: School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
authors: Fan
authors: F
authors: Mei
authors: Guhan
authors: G
authors: Nagappan
authors: Yang
authors: Y
authors: Ke
authors: Todd C
authors: TC
authors: Sacktor
authors: Bai
authors: B
authors: Lu
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D015971:Gene Expression Regulation, Enzymologic; D017774:Long-Term Potentiation; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D011493:Protein Kinase C / Q000096:biosynthesis / Q000378:metabolism*; D013997:Time Factors; D000099221:Protein Kinase C zeta
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D011493:Protein Kinase C; D000099221:Protein Kinase C zeta