The roles of protein expression in synaptic plasticity and memory consolidation

Abstract

The amount and availability of proteins are regulated by their synthesis, degradation, and transport. These processes can specifically, locally, and temporally regulate a protein or a population of proteins, thus affecting numerous biological processes in health and disease states. Accordingly, malfunction in the processes of protein turnover and localization underlies different neuronal diseases. However, as early as a century ago, it was recognized that there is a specific need for normal macromolecular synthesis in a specific fragment of the learning process, memory consolidation, which takes place minutes to hours following acquisition. Memory consolidation is the process by which fragile short-term memory is converted into stable long-term memory. It is accepted today that synaptic plasticity is a cellular mechanism of learning and memory processes. Interestingly, similar molecular mechanisms subserve both memory and synaptic plasticity consolidation. In this review, we survey the current view on the connection between memory consolidation processes and proteostasis, i.e., maintaining the protein contents at the neuron and the synapse. In addition, we describe the technical obstacles and possible new methods to determine neuronal proteostasis of synaptic function and better explain the process of memory and synaptic plasticity consolidation.

Activation of the G protein-coupled estrogen receptor, but not estrogen receptor α or β, rapidly enhances social learning

“…Estradiol may therefore act rapidly on early memory consolidation mechanisms through protein kinase cascades (Fortress et al, 2013;Sarkar et al, 2010;Srivastava, 2012) and/or by modifying dendritic spine morphology (Luine and Frankfurt, 2012;Phan et al, 2012;Srivastava, 2012). The effect observed here and by Phan et al (2012) at a time when memory consolidation is not yet completed (Rosenberg et al, 2014;Rudy, 2014) suggest that 17␤-E2 may also rapidly affect the early encoding of new memories.…”

Dynamics of Hippocampal Protein Expression During Long-term Spatial Memory Formation

“…Despite the abundant candidates involved even in a specific learning process, the actual number of neurons may be limited and a memory engram may be spatially curbed to specific subspaces of neurons. Learning is a dynamic process while protein expression and post-translational modification profiles may markedly change at different stages (33,72,73). Longterm synaptic plasticity is believed to be a cellular correlate of LTM.…”

“…Multiple synaptic activity-dependent signal transduction pathways (7)(8)(9)(10)(11)(12)(13)19) orchestrate the regulation of synaptic plasticity on the translational level (for review see (20,21)). Accumulated evidence shows that different types of LTM depend on protein synthesis, disregarding dependence on brain regions such as amygdala (22,23), hippocampus (24 -29), and medial prefrontal or insular cortex ((30 -32); for review see (33)). However, LTM perseveres significantly longer than duration of translation-dependent long-term plasticity.…”

Locus Coeruleus in time with the making of memories

“…To establish long term memory, post encoding cellular and molecular processes take place over several hours, involving activation of many intracellular signaling pathways, eventually leading to new protein synthesis and changes in synaptic weights in relevant brain regions [10]. This is known as 'molecular memory consolidation' [11].…”