Author(s): Shieh PB, Ghosh A, Shieh PB, Ghosh A
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Abstract Activity-dependent changes in synaptic strength, which appear to underlie cortical plasticity, require long-lasting biochemical changes in the postsynaptic neuron. An inductive event common to several forms of synaptic plasticity is an influx of calcium into the postsynaptic cell. Calcium acts as a second messenger to set into motion a cascade of biochemical signaling events that leads to new gene expression. Brain-derived neurotrophic factor (BDNF) is one such calcium-regulated gene that appears to be involved in activity-dependent cortical plasticity. Studies of the mechanism by which calcium influx induces BDNF expression have revealed that the BDNF promoter is regulated by two calcium response elements. One of the elements appears to be regulated by a novel transcription factor, while the other element is regulated by the previously characterized transcription factor CREB. The calcium signal is propagated to the CREB-mediated component of BDNF expression by CaM kinase IV. This signaling pathway, which links calcium influx to the induction of BDNF via CaM kinase IV and CREB, is likely to be centrally involved in mediating long-term activity-dependent plasticity. Copyright 1999 John Wiley & Sons, Inc.
This article was published in J Neurobiol
and referenced in Journal of Drug Metabolism & Toxicology