PRESYNAPTIC PLASTICITY IN THE AMYGDALA WITH FEAR CONDITIONING

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The consolidation of fear conditioning involves upregulation of numerous transcription factors and genes. This transcription is necessary for long-term memory formation and is subject to epigenetic regulation. Chromatin modifications play a dynamic role in fear conditioning and synaptic plasticity. In this study, we show that the Homer1a mRNA rapidly increases after fear conditioning in vivo and after BDNF application in vitro and that these increases are dependent on transcription and MAPK signaling. We then examine chromatin modifications of the Homer1a promoter after BDNF-induced plasticity of amygdala and hippocampal cultured cells and after fear consolidation in vivo. Interestingly, amygdala and hippocampal tissues appear to have differential regulation of chromatin around the homer1a promoter despite similar upregulation of mRNA after fear conditioning and BDNF induced plasticity. These data provide evidence for dynamic regulation of Homer1a following BDNF-induced plasticity or during BDNF-dependent learning process, and that upregulation of this gene is regulated through distinct epigenetic mechanisms in the hippocampus and amygdala.