作者: Martina Blank , Fernanda S. Petry , Martina Lichtenfels , Fernanda E. Valiati , Arethuza S. Dornelles
DOI: 10.1007/S00702-015-1464-7
关键词:
摘要: Relatively little is known about the requirement of signaling initiated by brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB), in early phases memory consolidation, as well possible functional interactions with epigenetic mechanisms. Here we show that blocking TrkB dorsal hippocampus after learning or retrieval impairs retention for inhibitory avoidance (IA). More importantly, impairing effect antagonism on consolidation was completely prevented histone deacetylase (HDAC) inhibitor sodium butyrate (NaB). Male Wistar rats were given an intrahippocampal infusion saline (SAL) NaB before training, followed either vehicle (VEH) selective antagonist ANA-12 immediately training. In a second experiment, infusions administered retrieval. training produced significant impairment subsequent test. Pretraining administration ANA-12, although did not alter resulting from blockade. The results indicate inhibition BDNF/TrkB can hinder reconsolidation IA memory. However, activity required presence NaB, suggesting dysfunction be fully compensated HDAC to allow hippocampal formation.