scholarly journals Lysosomes convene to keep the synapse clean

2017 ◽  
Vol 216 (8) ◽  
pp. 2251-2253 ◽  
Author(s):  
Natalia L. Kononenko
Keyword(s):  
Plasma Membrane ◽  
Protein Degradation ◽  
Neuronal Activity ◽  
Dendritic Spines ◽  
Acid Receptor ◽  
Synaptic Remodeling ◽  
Cell Biol ◽  
First Time ◽  
Local Protein

In neurons, lysosomes regulate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor levels at the plasma membrane, although their presence at distal dendrites is controversial. In this issue, Goo et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201704068) show for the first time that neuronal activity positions lysosomes at the dendritic spines to facilitate synaptic remodeling through local protein degradation.

scholarly journals More than a mere supply of monomers: G-Actin pools regulate actin dynamics in dendritic spines

2017 ◽  
Vol 216 (8) ◽  
pp. 2255-2257 ◽  
Author(s):  
Katalin Schlett
Keyword(s):  
Plasma Membrane ◽  
Dendritic Spines ◽  
Actin Polymerization ◽  
Synaptic Activity ◽  
Actin Dynamics ◽  
Actin Monomer ◽  
Cell Biol ◽  
Local Enrichment

Synaptic activity reshapes the morphology of dendritic spines via regulating F-actin arborization. In this issue, Lei et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201612042) reports a novel, G-actin–dependent regulation of actin polymerization within spine heads. They show that actin monomer levels are elevated in spines upon activity, with G-actin immobilized by the local enrichment of phosphatidylinositol (3,4,5)-triphosphate (PIP3) within the spine plasma membrane.

Transbilayer movement of fluorescent and spin-labeled phospholipids in the plasma membrane of human fibroblasts: a quantitative approach

1996 ◽  
Vol 109 (3) ◽  
pp. 687-698 ◽  
Author(s):  
T. Pomorski ◽  
P. Muller ◽  
B. Zimmermann ◽  
K. Burger ◽  
P.F. Devaux ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Initial Velocity ◽  
Plasma Membranes ◽  
Atp Hydrolysis ◽  
Human Fibroblasts ◽  
Atp Depletion ◽  
Aminophospholipid Translocase ◽  
Order Of Magnitude ◽  
Complicating Factors ◽  
First Time

All phospholipids in the plasma membrane of eukaryotic cells are subject to a slow passive transbilayer movement. In addition, aminophospholipids are recognized by the so-called aminophospholipid translocase, and are rapidly moved from the exoplasmic to the cytoplasmic leaflet of the plasma membrane at the expense of ATP hydrolysis. Though these principal pathways of transbilayer movement of phospholipids probably apply to all eukaryotic plasma membranes, studies of the actual kinetics of phospholipid redistribution have been largely confined to non-nucleated cells (erythrocytes). Experiments on nucleated cells are complicated by endocytosis and metabolism of the lipid probes inserted into the plasma membrane. Taking these complicating factors into account, we performed a detailed kinetic study of the transbilayer movement of short-chain fluorescent (N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl); NBD) and, for the first time, spin-labeled analogues of phosphatidylcholine (PC), -ethanolamine (PE), -serine (PS), and sphingomyelin (SM) in the plasma membrane of cultured human gingival fibroblasts. At 20 degrees C, the passive transbilayer diffusion of NBD analogues was very slow, and the choline-containing NBD analogues were internalized predominantly by endocytosis. Spin-labeled analogues of PC and SM showed higher passive transbilayer diffusion rates, and probably entered the cell by both passive transbilayer movement and endocytosis. In contrast, the rapid uptake of NBD- and spin-labeled aminophospholipid analogues could be mainly ascribed to the action of the aminophospholipid translocase, since it was inhibited by ATP depletion and N-ethylmaleimide pretreatment. The initial velocity of NBD-aminophospholipid translocation was eight to ten times slower than that of the corresponding spin-labeled lipid, and the half-times of redistribution of NBD-PS and spin-labeled PS were 7.2 and 3.6 minutes, respectively. Our data indicate that in human fibroblasts the initial velocity of aminophospholipid translocation is at least one order of magnitude higher than that in human erythrocytes, which should be sufficient to maintain the phospholipid asymmetry in the plasma membrane.

scholarly journals Neuronal receptors display cytoskeleton-independent directed motion on the plasma membrane

2018 ◽  
Author(s):  
R. D. Taylor ◽  
M. Heine ◽  
N. J. Emptage ◽  
L. C. Andreae
Keyword(s):  
Plasma Membrane ◽  
Neuronal Activity ◽  
Particle Tracking ◽  
Hippocampal Neurons ◽  
Intracellular Transport ◽  
Transmembrane Proteins ◽  
Single Particle Tracking ◽  
Directed Motion ◽  
Surface Movement ◽  
Transport Vesicles

AbstractDirected transport of transmembrane proteins is generally believed to occur via intracellular transport vesicles. However, using single particle tracking in rat hippocampal neurons with a pH-sensitive quantum dot probe which specifically reports surface movement of receptors, we have identified a subpopulation of neuronal EphB2 receptors that exhibit directed motion between synapses within the plasma membrane itself. This receptor movement occurs independently of the cytoskeleton but is dependent on cholesterol and is regulated by neuronal activity.

scholarly journals Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

2016 ◽  
Author(s):  
Tharkika Nagendran ◽  
Rylan S. Larsen ◽  
Rebecca L. Bigler ◽  
Shawn B. Frost ◽  
Benjamin D. Philpot ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Spine Density ◽  
Axon Injury ◽  
Synaptic Remodeling ◽  
Nerve Tracts ◽  
Specific Increase ◽  
Microfluidic Chambers

AbstractInjury of CNS nerve tracts remodels circuitry through dendritic spine loss and hyper-excitability, thus influencing recovery. Due to the complexity of the CNS, a mechanistic understanding of injury-induced synaptic remodeling remains unclear. Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presynaptic hyper-excitability. These remodeling events require activity at the site of injury, axon-to-soma signaling, and transcription. Similarly, directly injured corticospinal neurons in vivo also exhibit a specific increase in spiking following axon injury. Axotomy-induced hyper-excitability of cultured neurons coincides with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic spines. Netrin-1 downregulation occurs following axon injury and exogenous netrin-1 applied after injury normalizes spine density, presynaptic excitability, and inhibitory inputs at injured neurons. Our findings show that intrinsic signaling within damaged neurons regulates synaptic remodeling and involves netrin-1 signaling.

scholarly journals Light-induced engagement of microglia to focally remodel synapses in the adult brain

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Carla Cangalaya ◽  
Stoyan Stoyanov ◽  
Klaus-Dieter Fischer ◽  
Alexander Dityatev
Keyword(s):  
Transgenic Mice ◽  
Dendritic Spines ◽  
Adult Brain ◽  
Fluorescent Labels ◽  
Synaptic Remodeling ◽  
Presynaptic Boutons ◽  
Dependent Processes

Microglia continuously monitor synapses, but active synaptic remodeling by microglia in mature healthy brains is rarely directly observed. We performed targeted photoablation of single synapses in mature transgenic mice expressing fluorescent labels in neurons and microglia. The photodamage focally increased the duration of microglia-neuron contacts, and dramatically exacerbated both the turnover of dendritic spines and presynaptic boutons as well as the generation of new filopodia originating from spine heads or boutons. The results of microglia depletion confirmed that elevated spine turnover and the generation of presynaptic filopodia are microglia-dependent processes.

scholarly journals Microglia motility depends on neuronal activity and promotes structural plasticity in the hippocampus

2019 ◽  
Author(s):  
Felix C. Nebeling ◽  
Stefanie Poll ◽  
Lena C. Schmid ◽  
Manuel Mittag ◽  
Julia Steffen ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Dendritic Spines ◽  
Synapse Formation ◽  
Brain Parenchyma ◽  
Two Photon ◽  
Contact Rates ◽  
Health And Disease ◽  
The Impact ◽  
The Brain

AbstractMicroglia, the resident immune cells of the brain, play a complex role in health and disease. They actively survey the brain parenchyma by physically interacting with other cells and structurally shaping the brain. Yet, the mechanisms underlying microglia motility and their significance for synapse stability, especially during adulthood, remain widely unresolved. Here we investigated the impact of neuronal activity on microglia motility and its implication for synapse formation and survival. We used repetitive two-photon in vivo imaging in the hippocampus of awake mice to simultaneously study microglia motility and their interaction with synapses. We found that microglia process motility depended on neuronal activity. Simultaneously, more dendritic spines emerged in awake compared to anesthetized mice. Interestingly, microglia contact rates with individual dendritic spines were associated with their stability. These results suggest that microglia are not only sensing neuronal activity, but participate in synaptic rewiring of the hippocampus during adulthood, which has profound relevance for learning and memory processes.

scholarly journals Plasma membrane repairs by small GTPase Rab3a

2016 ◽  
Vol 213 (6) ◽  
pp. 613-615 ◽  
Author(s):  
Camilla Raiborg ◽  
Harald Stenmark
Keyword(s):  
Plasma Membrane ◽  
Small Gtpase ◽  
Membrane Repair ◽  
Cell Biol ◽  
Plasma Membrane Repair

Lysosomes fuse with the plasma membrane to help repair membrane lesions, but how they are positioned close to these lesions is not fully understood. Now, Encarnação et al. (2016. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201511093) demonstrate that the lysosomal GTPase Rab3a and its effectors orchestrate lysosome positioning and plasma membrane repair.

Comparative Aspects Of The Occluding Junctions In The Pulmonary And Bronchial Microcirculation

1981 ◽  
Author(s):  
H Bartels
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Freeze Fracture ◽  
Continuous System ◽  
Intramembranous Particles ◽  
Vasoactive Substances ◽  
Cell Biol ◽  
Occluding Junctions ◽  
Pulmonary Microcirculation

Compared with the pulmonary microcirculation the bronchial microcirculation reacts with a large increase in permeability after administration of vasoactive substances (Pietra et al., Cire. Res. 29, 323, 1971). Thus the occluding junctions between the endothelial cells of the rat pulmonary and bronchial microcirculation were investigated by means of freeze-fracture replicas in order to establish differences in their substructure which could be responsible for the different permeability properties. The prevailing feature of the occluding junctions between the endothelial cells of the pulmonary microvascular bed was a continuous system of anastomosing membrane foldings,carrying rows of intramembranous particles, which were usually located on face E of the split plasma membrane. This type of occluding junction is characteristic of capillaries (Simionescu et al., J. Cell Biol. 67, 863, 1975) . In the bronchial microcirculation many of the endothelial occluding junctions showed discontinuous assemblies of membrane foldings, which were lacking particles on face E. This type of “open” junction is typically localized at the venular end of the microvascular bed and susceptible to vasoactive substances (Simionescu et al., J. Cell Biol. 78, 27, 1978). It is suggested that the different permeability properties of the pulmonary and bronchial microcirculation is due to the large amount of postcapillary venules with their morphologically and functionally characteristic occluding junctions.

scholarly journals Maf1 regulates dendritic morphogenesis and influences learning and memory

2020 ◽  
Vol 11 (7) ◽  
Author(s):  
Kui Chen ◽  
Liang Zhu ◽  
Lin Guo ◽  
Yuan-Bo Pan ◽  
Dong-Fu Feng
Keyword(s):  
Learning And Memory ◽  
Dendritic Spines ◽  
Mtor Signaling ◽  
Pten Expression ◽  
Luciferase Reporter ◽  
Downstream Effector ◽  
Dendritic Morphogenesis ◽  
First Time

Abstract Maf1, a general transcriptional regulator and mTOR downstream effector, is highly expressed in the hippocampus and cortex, but the function of Maf1 in neurons is not well elucidated. Here, we first demonstrate that Maf1 plays a central role in the inhibition of dendritic morphogenesis and the growth of dendritic spines both in vitro and in vivo. Furthermore, Maf1 downregulation paradoxically leads to activation of AKT-mTOR signaling, which is mediated by decreased PTEN expression. Moreover, we confirmed that Maf1 could regulate the activity of PTEN promoter by luciferase reporter assay, and proved that Maf1 could bind to the promoter of PTEN by ChIP-PCR experiment. We also demonstrate that expression of Maf1 in the hippocampus affects learning and memory in mice. Taken together, we show for the first time that Maf1 inhibits dendritic morphogenesis and the growth of dendritic spines through AKT-mTOR signaling by increasing PTEN expression.

scholarly journals GTP-tubulin loves microtubule plus ends but marries the minus ends

2019 ◽  
Vol 218 (9) ◽  
pp. 2822-2823 ◽  
Author(s):  
Linda Wordeman
Keyword(s):  
Cell Biol ◽  
First Time

Microtubule minus ends are inherently more stable than plus ends despite the fact that free tubulin associates more avidly to the plus end. In this issue, Strothman et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201905019) measure, for the first time, the off-rate for GTP-tubulin and find that it is different for the two ends, suggesting that this parameter may control the transition to disassembly at microtubule ends.

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