Parvalbumin‐expressing ependymal cells in rostral lateral ventricle wall adhesions contribute to aging‐related ventricle stenosis in mice

Filice, Federica; Celio, Marco R.; Babalian, A.; Blum, Walter; Szabolcsi, Viktória

doi:10.1002/cne.24276

Cited by 12 publications

(17 citation statements)

References 46 publications

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“…The specificity of the guinea-pig anti-S100β antibody 287004 was tested by the provider (Synaptic Systems) using immunocytochemistry and western blots on cells transfected with the S100β sequence and on brain slices. Its specificity was further confirmed using western blot analysis (Filice et al 2017). The staining obtained in brain sections was reported to be similar to that obtained with another antibody directed against S100β raised in rabbit (Filice et al 2017).…”

Section: /79supporting

confidence: 63%

“…Its specificity was further confirmed using western blot analysis (Filice et al 2017). The staining obtained in brain sections was reported to be similar to that obtained with another antibody directed against S100β raised in rabbit (Filice et al 2017). The specificity of the goat anti-GFP antibody AB5450 was tested by the provider (Abcam) using immunoprecipitation and immunocytochemistry on transfected cells and on brain slices.…”

Section: /79mentioning

confidence: 60%

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Astrocytic modulation of information processing by layer 5 pyramidal neurons of the mouse visual cortex

Ryczko

Hanini-Daoud

Condamine

et al. 2020

Preprint

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AbstractThe most complex cerebral functions are performed by the cortex which most important output is carried out by its layer 5 pyramidal neurons. Their firing reflects integration of sensory and contextual information that they receive. There is evidence that astrocytes influence cortical neurons firing through the release of gliotransmitters such as ATP, glutamate or GABA. These effects were described at the network and at the synaptic levels, but it is still unclear how astrocytes influence neurons input-output transfer function at the cellular level. Here, we used optogenetic tools coupled with electrophysiological, imaging and anatomical approaches to test whether and how astrocytic activation affected processing and integration of distal inputs to layer 5 pyramidal neurons (L5PN). We show that optogenetic activation of astrocytes near L5PN cell body prolonged firing induced by distal inputs to L5PN and potentiated their ability to trigger spikes. The observed astrocytic effects on L5PN firing involved glutamatergic transmission to some extent but relied on release of S100β, an astrocytic Ca2+-binding protein that decreases extracellular Ca2+ once released. This astrocyte-evoked decrease of extracellular Ca2+ elicited firing mediated by activation of Nav1.6 channels. Our findings suggest that astrocytes contribute to the cortical fundamental computational operations by controlling the extracellular ionic environment.Key Points SummaryIntegration of inputs along the dendritic tree of layer 5 pyramidal neurons is an essential operation as these cells represent the most important output carrier of the cerebral cortex. However, the contribution of astrocytes, a type of glial cell to these operations is poorly documented.Here we found that optogenetic activation of astrocytes in the vicinity of layer 5 in the mouse primary visual cortex induce spiking in local pyramidal neurons through Nav1.6 ion channels and prolongs the responses elicited in these neurons by stimulation of their distal inputs in cortical layer 1.This effect partially involved glutamatergic signalling but relied mostly on the astrocytic calcium-binding protein S100β, which regulates the concentration of calcium in the extracellular space around neurons.These findings show that astrocytes contribute to the fundamental computational operations of the cortex by acting on the ionic environment of neurons.

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Section: /79supporting

confidence: 63%

Section: /79mentioning

confidence: 60%

Astrocytic modulation of information processing by layer 5 pyramidal neurons of the mouse visual cortex

Ryczko

Hanini-Daoud

Condamine

et al. 2020

Preprint

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“…Loading was controlled using Ponceau S staining and membranes were blocked with 5% milk in 0.1% Tween 20 in TBS for 1 h at room temperature and incubated overnight at 4 °C with rabbit polyclonal antibody PV-25 (Swant, Marly, Switzerland) at 1:5,000, or mouse monoclonal COX I antibody (ThermoFisher, Switzerland) at 1:1,000, respectively. The PV-25 antibody has been validated for Western blot analysis in our previous study 20 . Horseradish peroxidase (HRP)-conjugated goat anti-rabbit antibody or goat anti-mouse antibody (Sigma-Aldrich, Buchs, Switzerland) were added at a dilution of 1:10,000 for 2 h at room temperature.…”

Section: Methodsmentioning

confidence: 99%

“…However, following brain injury we observed upregulation of PV in ependymal cells and reactive astrocytes. Ependymal cells react with prompt and persistent PV-upregulation to invasive injury inflicted onto the lateral ventricle wall 19 and in aging-related lateral ventricle wall stenosis 20 . We demonstrated that injury-induced PV overexpression in ependymal cells was dependent on NF-κB signaling and was modulated by altering the level of oxidative stress, which implicates inflammation induced by injury in this process.…”

Section: Introductionmentioning

confidence: 99%

Parvalbumin expression in oligodendrocyte-like CG4 cells causes a reduction in mitochondrial volume, attenuation in reactive oxygen species production and a decrease in cell processes’ length and branching

Lichvarova

Blum

Schwaller

et al. 2019

Sci Rep

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Forebrain glial cells - ependymal cells and astrocytes -acquire upon injury- a “reactive” phenotype associated with parvalbumin (PV) upregulation. Since free radicals, e.g. reactive oxygen species (ROS) play a role in the pathogenesis of multiple sclerosis, and that PV-upregulation in glial cells is inversely correlated with the level of oxidative stress, we hypothesized that PV-upregulation might also protect oligodendrocytes by decreasing ROS production. Lentiviral transduction techniques allowed for PV overexpression in CG4 oligodendrocyte progenitor cells (OPCs). Depending on the growth medium CG4 cells can be maintained in an OPC-like state, or induced to differentiate into an oligodendrocyte (OLG)-like phenotype. While increased levels of PV had no effect on cell proliferation and invasiveness in vitro , PV decreased the mitochondria volume in CG4 cell bodies, as well as the mitochondrial density in CG4 processes in both OPC-like and OLG-like states. In line with the PV-induced global decrease in mitochondrial volume, elevated PV levels reduced transcript levels of mitochondrial transcription factors involved in mitochondria biogenesis. In differentiated PV-overexpressing CG4 cells with a decreased mitochondrial volume, UV-induced ROS production was lower than in control CG4 cells hinting towards a possible role of PV in counteracting oxidative stress. Unexpectedly, PV also decreased the length of processes in undifferentiated CG4 cells and moreover diminished branching of differentiated CG4 cell processes, strongly correlated with the decreased density of mitochondria in CG4 cell processes. Thus besides conferring a protective role against oxidative stress, PV in a cell autonomous fashion additionally affects process’ growth and branching in CG4 cells.

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“…In mutant brains, however, the regions lacking S100  ependymal cells were increased . We also used another marker, parvalbumin (PV), which is specifically expressed in ependymal cells at the stenosed region (Filice et al, 2017), and found that PV-positive cells were increased in mutant brains ( Figures S2A and S2B), confirming the enhanced stenosis in mutant brains. These results indicate that CAMSAP3 mutation promotes ventricular stenosis or fusion at the boundaries between the striatum and septum.…”

Section: Increased Ventricle Stenosis and Fusion In Camsap3 Mutant Brmentioning

confidence: 64%

CAMSAP3 is required for mTORC1-dependent ependymal cell growth and lateral ventricle shaping in mouse brains

Kimura

Saito

Kawsaki

et al. 2020

Preprint

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Microtubules (MTs) regulate numerous cellular processes, but their roles in brain morphogenesis are not well known. Here we show that CAMSAP3, a non-centrosomal microtubule regulator, is important for shaping the lateral ventricles. In differentiating ependymal cells, CAMSAP3 became concentrated at the apical domains, serving to generate MT networks at these sites. Camsap3-mutated mice showed abnormally narrow lateral ventricles, in which excessive stenosis or fusion was induced, leading to a decrease of neural stem cells at the ventricular and subventricular zones. This defect was ascribed at least in part to a failure of neocortical ependymal cells to broaden their apical domain, a process necessary for expanding the ventricular cavities. mTORC1 was required for ependymal cell growth but its activity was downregulated in mutant cells. Lysosomes, which mediate mTORC1 activation, tended to be reduced at the apical regions of the mutant cells, along with disorganized apical MT networks at the corresponding sites. These findings suggest that CAMSAP3 supports mTORC1 signaling required for ependymal cell growth via MT network regulation, and, in turn, shaping of the lateral ventricles.

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Parvalbumin‐expressing ependymal cells in rostral lateral ventricle wall adhesions contribute to aging‐related ventricle stenosis in mice

Cited by 12 publications

References 46 publications

Astrocytic modulation of information processing by layer 5 pyramidal neurons of the mouse visual cortex

Astrocytic modulation of information processing by layer 5 pyramidal neurons of the mouse visual cortex

Parvalbumin expression in oligodendrocyte-like CG4 cells causes a reduction in mitochondrial volume, attenuation in reactive oxygen species production and a decrease in cell processes’ length and branching

CAMSAP3 is required for mTORC1-dependent ependymal cell growth and lateral ventricle shaping in mouse brains

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