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Acetylation of Nuclear Factor-B in Rat Amygdala Improves Long-Term but not Short-Term Retention of Fear Memory

Institute of Basic Medical Sciences and Department of Pharmacology, College of Medicine, National Cheng-Kung University, Tainan (S.-H.Y., C.-H.L., P.-W.G.); and School of Pharmacy, China Medical University, Taichung, Taiwan (P.-W.G.)

Memory consolidation is mediated by new protein synthesis. However, the transcriptional pathways induced in neurons by behavioral training that activate gene responses have yet to be fully delineated. We have previously shown that nuclear factor B (NF-B) is activated in the amygdala after fear conditioning. Here we report that fear conditioning resulted in an increase in histone acetyl-transferase activity, the association between NF-B p65 and CBP, and the increase in acetylated p65. Pretreating animals with histone deacetylase (HDAC) inhibitors prolonged the nuclear expression of acetyl-p65 and increased its DNA binding activity. Consistent with these results, HDAC inhibitors enhanced long-term but not short-term fear memory, and this effect was attenuated by B decoy DNA, whereas scrambled DNA was without effect. This study provides evidence that HDAC-mediated deacetylation functions as an intranuclear molecular switch culminating in the termination of NF-B transcriptional response that is involved in the formation of fear memory.

Received August 25, 2003; accepted February 9, 2004.

Address correspondence to: Po-Wu Gean, School of Pharmacy, China Medical University, Taichung, Taiwan 404. E-mail: pwgean{at}mail.cmu.edu.tw

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