Update bibliography

_bibliography/papers.bib

@@ -4,6 +4,7 @@
 @string{aps = {American Physical Society,}}
 
 @article{dzyubenko_role_2018,
+  abbr={TAND},
 	title = {Role of immune responses for extracellular matrix remodeling in the ischemic brain},
 	volume = {11},
 	issn = {1756-2864, 1756-2864},
@@ -21,6 +22,7 @@ @article{dzyubenko_role_2018
 }
 
 @misc{manrique-castano_dissecting_2023,
+  abbr={BioArx},
 	title = {Dissecting glial scar formation by spatial point pattern and topological data analysis},
 	copyright = {© 2023, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution 4.0 International), CC BY 4.0, as described at http://creativecommons.org/licenses/by/4.0/},
 	url = {https://www.biorxiv.org/content/10.1101/2023.10.04.560910v1},
@@ -38,7 +40,7 @@ @misc{manrique-castano_dissecting_2023
 }
 
 @article{dzyubenko_topological_2018,
-  abbr={Matrix Biology},
+  abbr={MatBio},
   title={Topological remodeling of cortical perineuronal nets in focal cerebral ischemia and mild hypoperfusion},
   author={Dzyubenko, Egor and Manrique-Castano, Daniel and Kleinschnitz, Christoph and Faissner, Andreas and Hermann, Dirk M.},
   abstract={Despite the crucial role of perineuronal nets (PNNs) in neural plasticity and neurological disorders, their ultrastructural organization remains largely unresolved. We have developed a novel approach combining superresolution structured illumination microscopy (SR-SIM) and mathematical reconstruction that allows for quantitative analysis of PNN topology. Since perineuronal matrix is capable to restrict neural plasticity but at the same time is necessary to maintain synapses, we hypothesized that a beneficial post stroke recovery requires a reversible loosening of PNNs. Our results indicated that focal cerebral ischemia induces partial depletion of PNNs and that mild hypoperfusion not associated with ischemic injury can induce ultra-structural rearrangements in visually intact meshworks. In line with the activation of neural plasticity under mild stress stimuli, we provide evidence that topological conversion of PNNs can support post stroke neural rewiring.},
@@ -59,6 +61,7 @@ @article{dzyubenko_topological_2018
 }
 
 @article{dzyubenko_tenascin-c_2022,
+  abbr={MatBio},
 	title = {Tenascin-{C} restricts reactive astrogliosis in the ischemic brain},
 	volume = {110},
 	issn = {0945-053X},
@@ -76,6 +79,7 @@ @article{dzyubenko_tenascin-c_2022
 }
 
 @article{daniel_manrique-castano_neurovascular_2021,
+  abbr={Exxon},
 	title = {Neurovascular {Reactivity} in {Tissue} {Scarring} {Following} {Cerebral} {Ischemia}},
 	copyright = {Copyright (c) 2021 Daniel Manrique-Castano, PHD, Ayman ElAli, PHD},
 	url = {https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-neurovascular-reactivity},
@@ -94,6 +98,7 @@ @article{daniel_manrique-castano_neurovascular_2021
 }
 
 @article{lecordier_neurovascular_2021,
+	abbr={Front. cell. neurosci},
 	title = {Neurovascular {Alterations} in {Vascular} {Dementia}: {Emphasis} on {Risk} {Factors}},
 	volume = {13},
 	issn = {1663-4365},
@@ -107,11 +112,40 @@ @article{lecordier_neurovascular_2021
 	pdf = {Lecordier et al. - 2021 - Neurovascular Alterations in Vascular Dementia Em.pdf},
 }
 
-@book{przibram1967letters,
-  bibtex_show={true},
-  title={Letters on wave mechanics},
-  author={Einstein, Albert and Schrödinger, Erwin and Planck, Max and Lorentz, Hendrik Antoon and Przibram, Karl},
-  year={1967},
-  publisher={Vision},
-  preview={wave-mechanics.gif}
+@article{dzyubenko_inhibitory_2021,
+  abbr={CMLS}, 
+	title = {Inhibitory control in neuronal networks relies on the extracellular matrix integrity},
+	volume = {78},
+	issn = {1420-9071},
+	url = {https://doi.org/10.1007/s00018-021-03861-3},
+	doi = {10.1007/s00018-021-03861-3},
+	abstract = {Inhibitory control is essential for the regulation of neuronal network activity, where excitatory and inhibitory synapses can act synergistically, reciprocally, and antagonistically. Sustained excitation-inhibition (E-I) balance, therefore, relies on the orchestrated adjustment of excitatory and inhibitory synaptic strength. While growing evidence indicates that the brain’s extracellular matrix (ECM) is a crucial regulator of excitatory synapse plasticity, it remains unclear whether and how the ECM contributes to inhibitory control in neuronal networks. Here we studied the simultaneous changes in excitatory and inhibitory connectivity after ECM depletion. We demonstrate that the ECM supports the maintenance of E-I balance by retaining inhibitory connectivity. Quantification of synapses and super-resolution microscopy showed that depletion of the ECM in mature neuronal networks preferentially decreases the density of inhibitory synapses and the size of individual inhibitory postsynaptic scaffolds. The reduction of inhibitory synapse density is partially compensated by the homeostatically increasing synaptic strength via the reduction of presynaptic GABAB receptors, as indicated by patch-clamp measurements and GABAB receptor expression quantifications. However, both spiking and bursting activity in neuronal networks is increased after ECM depletion, as indicated by multi-electrode recordings. With computational modelling, we determined that ECM depletion reduces the inhibitory connectivity to an extent that the inhibitory synapse scaling does not fully compensate for the reduced inhibitory synapse density. Our results indicate that the brain’s ECM preserves the balanced state of neuronal networks by supporting inhibitory control via inhibitory synapse stabilization, which expands the current understanding of brain activity regulation.},
+	language = {en},
+	number = {14},
+	urldate = {2024-03-01},
+	journal = {Cellular and Molecular Life Sciences},
+	author = {Dzyubenko, Egor and Fleischer, Michael and Manrique-Castano, Daniel and Borbor, Mina and Kleinschnitz, Christoph and Faissner, Andreas and Hermann, Dirk M.},
+	month = jul,
+	year = {2021},
+	keywords = {E-I balance, ECM, Electrophysiology, Inhibitory synapse, Neuronal network activity},
+	pages = {5647--5663},
+	pdf = {Dzyubenko et al. - 2021 - Inhibitory control in neuronal networks relies on .pdf},
+}
+
+@article{manrique-castano_tenascin-c_2021,
+  abbr={BBI}, 
+	title = {Tenascin-{C} preserves microglia surveillance and restricts leukocyte and, more specifically, {T} cell infiltration of the ischemic brain},
+	volume = {91},
+	issn = {0889-1591},
+	url = {https://www.sciencedirect.com/science/article/pii/S0889159120323667},
+	doi = {10.1016/j.bbi.2020.10.016},
+	abstract = {As an endogenous activator of toll-like receptor-4 (Tlr4), the extracellular matrix glycoprotein tenascin-C (TnC) regulates chemotaxis, phagocytosis and proinflammatory cytokine production in microglia. The role of TnC for ischemic brain injury, post-ischemic immune responses and stroke recovery has still not been evaluated. By comparing wild type and TnC−/− mice exposed to transient intraluminal middle cerebral artery occlusion (MCAO), we examined the effects of TnC deficiency for ischemic injury, neurological deficits, microglia/macrophage activation and brain leukocyte infiltration using behavioural tests, histochemical studies, Western blot, polymerase chain reaction and flow cytometry. Histochemical studies revealed that TnC was de novo expressed in the ischemic striatum, which contained the infarct core, and overlapped with the area of strongest accumulation of Iba1 + microglia/macrophages. TnC deficiency increased overall Iba1 immunoreactivity in the perilesional cortex, suggesting that TnC might restrict the distribution of microglial cells to the infarct core. By analysing microglial morphology in 3D we found that the post-ischemic loss of microglial cell territory, branching and volume at 3 and 7 days post-ischemia was amplified in the brains of TnC deficient compared with wild type mice. Microglial cell number was not different between genotypes. Hence, TnC deficiency reduced tissue surveillance by microglial cells. Concomitantly, the number of infiltrating leukocytes and, more specifically, T cells was increased in the ischemic brain parenchyma of TnC deficient compared with wild type mice. Ischemic injury and neurological deficits were not affected by TnC deficiency. We propose that the reduced microglia surveillance in TnC deficient mice might favour leukocyte accumulation in the ischemic brain.},
+	urldate = {2024-03-01},
+	journal = {Brain, Behavior, and Immunity},
+	author = {Manrique-Castano, Daniel and Dzyubenko, Egor and Borbor, Mina and Vasileiadou, Paraskevi and Kleinschnitz, Christoph and Roll, Lars and Faissner, Andreas and Hermann, Dirk M.},
+	month = jan,
+	year = {2021},
+	keywords = {Extracellular matrix, Focal cerebral ischemia, Microglial activation, TnC},
+	pages = {639--648},
+	pdf = {Tenascin-C preserves microglia surveillance and restricts leukocyte.pdf}
 }