A tiny detail visible on certain neurons at the limit of resolution in light microscopy went in 130 years of neuroscience research through a dazzling career from suspicious staining artifact to what we recognize today as a complex postsynaptic molecular machine: the dendritic spine.This chapter deals with techniques to make spines visible. The original technique, Golgi silver staining, is still being used today. Electron microscopy and automated field ion beam scanning electron microscopy are ultrahigh resolution techniques, albeit specialized. Other methods are intracellular injection, uptake of dyes, and recently the exploitation of genetically modified animals in which certain neurons express fluorescent protein in all their processes, including the nooks and crannies of their dendritic spines.
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http://dx.doi.org/10.1007/978-3-031-36159-3_2 | DOI Listing |
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 PDFJ Comp Neurol
January 2025
Graduate Program in Molecular and Systems Pharmacology, Emory University, Atlanta, Georgia, USA.
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 PDFFood 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 PDFSci 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 PDFProc Natl Acad Sci U S A
January 2025
Center for Neuroscience, University of California, Davis, CA 95618.
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.
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