Imaging dendritic spines: molecular organization and signaling for plasticity.

Curr Opin Neurobiol

Program in Neuroscience and Behavioral Disorders, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore. Electronic address:

Published: April 2021

The structural plasticity of dendritic spines is considered to be essential for various forms of synaptic plasticity and, ultimately, learning and memory. The process is mediated by signaling pathways that promote the reorganization of the actin cytoskeleton and subsynaptic structures, which in turn cause structural and functional changes in dendritic spines. Recent advances in optical technologies have started to reveal the fine molecular structures and dynamic signaling occurring inside spines, providing significant insights into the molecular regulation of spines. Here, we highlight recent studies to resolve the molecular mechanisms underlying the spine actin cytoskeleton and plasticity with high spatiotemporal resolution. Moreover, we discuss new genome editing-based approaches in imaging the molecular structure and plasticity of dendritic spines.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.conb.2020.08.006DOI Listing

Publication Analysis

Top Keywords

dendritic spines
16
plasticity dendritic
8
actin cytoskeleton
8
spines
6
molecular
5
plasticity
5
imaging dendritic
4
spines molecular
4
molecular organization
4
organization signaling
4

Similar Publications

ATAD1 Regulates Neuronal Development and Synapse Formation Through Tuning Mitochondrial Function.

Int J Mol Sci

December 2024

Hefei National Laboratory for Physical Sciences at the Microscale, MOE Key Laboratory for Membrane-Less Organelles & Cellular Dynamics, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230026, China.

Mitochondrial function is essential for synaptic function. ATAD1, an AAA+ protease involved in mitochondrial quality control, governs fission-fusion dynamics within the organelle. However, the distribution and functional role of ATAD1 in neurons remain poorly understood.

View Article and Find Full Text PDF

Glutamate delta receptor 1 (GluD1) is a unique synaptogenic molecule expressed at excitatory and inhibitory synapses. The lateral habenula (LHb), a subcortical structure that regulates negative reward prediction error and major monoaminergic systems, is enriched in GluD1. LHb dysfunction has been implicated in psychiatric disorders such as depression and schizophrenia, both of which are associated with GRID1, the gene that encodes GluD1.

View Article and Find Full Text PDF

Melatonin attenuates BDE-209-caused spatial memory deficits in juvenile rats through NMDAR-CaMKⅡγ-mediated synapse-to-nucleus signaling.

Food Chem Toxicol

January 2025

Department of Occupational and Environmental Health, School of Public Health, Jinzhou Medical University, Jinzhou, Liaoning, PR China. Electronic address:

Flame retardant polybrominated diphenyl ethers (PBDEs) accumulate in human bodies through food and dust ingestion, and cause neurobehavioral deficits with obscure mechanism. We aimed to investigate NMDAR-CaMKⅡγ-mediated synapse-to-nuclear communication involved in BDE-209-induced cognitive impairment, and alleviation from exogenous melatonin. Decreased NMDAR subunits GluN2A and 2B, autophosphorylation of CaMKⅡα, and postsynaptic GluA1 trafficking were observed in the hippocampus of juvenile rats after maternal BDE-209 exposure.

View Article and Find Full Text PDF

Hippocampal dendritic spines store-operated calcium entry and endoplasmic reticulum content is dynamic microtubule dependent.

Sci Rep

January 2025

Laboratory of Biomedical Imaging and Data Analysis, Institute of Biomedical Systems and Biotechnology, Peter the Great St. Petersburg Polytechnic University, Khlopina St. 11, St. Petersburg, Russia, 194021.

One of the mechanisms of calcium signalling in neurons is store-operated calcium entry (SOCE), which is activated when the calcium concentration in the smooth endoplasmic reticulum (ER) decreases and its protein-calcium sensor STIM (stromal interacting molecule) relocate to the endoplasmic reticulum and plasma membrane junctions, forms clusters and induces calcium entry. In electrically non-excitable cells, STIM1 is coupled with the positive end of a tubulin microtubule through interaction with EB1 (end-binding) protein, which controls its oligomerization, SOCE and participates in ER movement. STIM2 homologue, which is specific for mature hippocampal dendritic spines, is known to interact with EB3 protein, however, not much is known about the role of this interaction in STIM2 clustering or ER trafficking in neurons.

View Article and Find Full Text PDF

How newly formed memories are preserved while brain plasticity is ongoing has been a source of debate. One idea is that synapses which experienced recent plasticity become resistant to further plasticity, a type of metaplasticity often referred to as saturation. Here, we probe the local dendritic mechanisms that limit plasticity at recently potentiated synapses.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!