Long-Term Potentiation-Associated Gene Expression: Involvement of the Tumour Protein p53

Long-term potentiation of synaptic transmission (LTP) is one of the most studied manifestations of neuroplasticity and hippocampus is a classic object for the study of LTP mechanisms. The early phase of LTP depends on modifications of pre-existing synaptic proteins and the late phase of LTP needs de novo protein synthesis and gene expression. LTP-associated dynamics of the transcriptome and mechanisms of coupling synaptic activity with gene expression are intensively studied, but due to the vast complexity of the issue, abundance of unresolved questions remains in this field. The diversity of brain cell types is one of the main challenges. Until relatively recently, the analysis of molecular and genetic aspects of neuroplasticity has usually been confined to neuronal populations. Meanwhile, glia substantially contributes to synaptic transmission regulation. Astrocytes release various gliotransmitters, which modulate synaptic transmission and plasticity. S100B is one of those glia-derived regulatory factors. Learning in rats is accompanied by an increase in S100B expression in various brain regions including the hippocampus. The present study is focused on the neuroplasticity-associated S100B expression upregulation using long-term post-tetanic potentiation in rat hippocampal slices. In this chapter, we present a short review of published articles devoted to the analysis of gene expression during LTP formation including studies of the mechanism of LTP-associated S100B upregulation in hippocampus