Actin remodeling, the synaptic tag and the maintenance of synaptic plasticity

Abstract

Activity‐dependent plasticity of synaptic connections is a hallmark of the mammalian brain and represents a key mechanism for rewiring neural circuits during development, experience‐dependent plasticity, and brain disorders. Cellular models of memory, such as long‐term potentiation and long‐term depression, share common principles to memory consolidation. As for memory, the maintenance of synaptic plasticity is dependent on the synthesis of de novo protein synthesis. The synaptic‐tagging and capture hypothesis states that the maintenance of synaptic plasticity is dependent on the interplay between input‐specific synaptic tags and the allocation or capture of plasticity‐related proteins (PRPs) at activated synapses. The setting of the synaptic tag and the capture of PRPs are independent processes that can occur separated in time and different groups of activated synapses. How are these two processes orchestrated in time and space? Here, we discuss the synaptic‐tagging and capture hypothesis in the light of neuronal compartmentalization models and address the role of actin as a putative synaptic tag. If different groups of synapses interact by synaptic‐tagging and capture mechanisms, understanding the spatial rules of such interaction is key to define the relevant neuronal compartment. We also discuss how actin modulation can allow an input‐specific capture of PRPs and try to conciliate the temporal dynamics of synaptic actin with the maintenance of plasticity. Understanding how multiple synapses interact in time and space is fundamental to predict how neurons integrate information and ultimately how memory is acquired.

Differentially Expressed Circular RNAs in Peripheral Blood Mononuclear Cells of Patients with Parkinson's Disease

“…To explore the molecular pathways controlled by the five miRNAs, we performed in silico analysis of KEGG pathways and GOslim terms. KEGG categories revealed multiple signaling pathways (thyroid hormone, phosphatidylinositol, MAPK, FoxO) implicated in neuronal survival and plasticity and “Regulation of actin cytoskeleton,” which is central to presynaptic and postsynaptic assembly as overrepresented 78‐81 . GOslim analysis revealed “cellular protein modification,” “nucleic acid binding transcription factor activity,” “cytoskeletal protein binding,” “cell death,” and “response to stress” as overrepresented among the biological processes affected.…”

Dendritic Spine Plasticity: Function and Mechanisms

“…One big question is how only stimulated spines can be selectively provided with plasticity-related proteins when activity-induced transcription typically changes gene expression in the whole cell. A body of studies indicates that activity-dependent mRNAs and proteins can preferentially be transported and captured at stimulated spines for local translation via a synaptic tagging and capture mechanism ( Figure 3 ) that remains to be elucidated (Martin et al, 1997 ; Martin and Kosik, 2002 ; Redondo and Morris, 2011 ; Okuno et al, 2012 ; Pinho et al, 2020 ).…”

Reduced PTPRD expression differentially alters brain phosphotyrosine phosphoproteomic profiles of 2 and 12 month-old mice

“…Supporting studies of PTPRD phosphatase activities: We synthesized several actin as well as cofilin and dock4 phosphopeptides as candidate substrates for PTPRD's phosphatase since these were: a) among those whose abundance increased most strikingly in two month old mice with reduced PTPRD expression; b) products of genes that are coexpressed abundantly with PTPRD in cerebral cortical neuronal cell types and c) products of genes that are good candidates for involvement in neuronal adaptations plausibly associated with PTPRD functions as a synaptic organizer (3,(25)(26)(27)(28).…”