Publications by authors named "Rusakov D"

This study explores the innovative potential of native lignin as a sustainable biopolyol for synthesizing polyurethane aerogels with variable microstructures, significant specific surface areas, and high mechanical stability. Three types of lignin-Organosolv, Aquasolv, and Soda lignin-were evaluated based on structural characteristics, Klason lignin content, and particle size, with Organosolv lignin being identified as the optimal candidate. The microstructure of lignin polyurethane samples was adjustable by solvent choice: Gelation in DMSO and pyridine, with high affinity to lignin, resulted in dense materials with low specific surface areas, while the use of the low-affinity solvent e.

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Brain computation performed by billions of nerve cells relies on a sufficient and uninterrupted nutrient and oxygen supply. Astrocytes, the ubiquitous glial neighbours of neurons, govern brain glucose uptake and metabolism, but the exact mechanisms of metabolic coupling between neurons and astrocytes that ensure on-demand support of neuronal energy needs are not fully understood. Here we show, using experimental in vitro and in vivo animal models, that neuronal activity-dependent metabolic activation of astrocytes is mediated by neuromodulator adenosine acting on astrocytic A2B receptors.

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Which proportion of the long-term potentiation (LTP) expressed in the bulk of excitatory synapses is postsynaptic and which presynaptic remains debatable. To understand better the possible impact of either LTP form, we explored a realistic model of a CA1 pyramidal cell equipped with known membrane mechanisms and multiple, stochastic excitatory axo-spinous synapses. Our simulations were designed to establish an input-output transfer function, the dependence between the frequency of presynaptic action potentials triggering probabilistic synaptic discharges and the average frequency of postsynaptic spiking.

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Neutrophils are white blood cells that are critical to acute inflammatory and adaptive immune responses. Their swarming-pattern behavior is controlled by multiple cellular cascades involving calcium-dependent release of various signaling molecules. Previous studies have reported that neutrophils express glutamate receptors and can release glutamate but evidence of direct neutrophil-neutrophil communication has been elusive.

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Once outside the synaptic cleft, the excitatory neurotransmitter glutamate is rapidly bound by its high-affinity transporters, which are expressed in abundance on the surface of perisynaptic astroglia. While this binding and the subsequent uptake of glutamate constrain excitatory transmission mainly within individual synapses, there is growing evidence for the physiologically important extrasynaptic actions of glutamate. However, the mechanistic explanation and the scope of such actions remain obscure.

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Mechanisms that entrain and pace rhythmic epileptiform discharges remain debated. Traditionally, the quest to understand them has focused on interneuronal networks driven by synaptic GABAergic connections. However, synchronized interneuronal discharges could also trigger the transient elevations of extracellular GABA across the tissue volume, thus raising tonic conductance (G) of synaptic and extrasynaptic GABA receptors in multiple cells.

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Article Synopsis
  • Mutations in the SNCA gene are linked to autosomal dominant Parkinson's disease (PD), leading to the degeneration of dopaminergic neurons and the formation of α-synuclein aggregates.
  • Using human-induced pluripotent stem cells (hiPSCs), researchers identified the early pathophysiological events triggered by SNCA mutations, revealing the initial formation of small aggregates before the development of mature midbrain dopaminergic neurons.
  • The study found that early disruptions in calcium signaling and mitochondrial dysfunction occurred as the disease progressed, ultimately resulting in altered neuronal activity and cell death, highlighting the role of protein misfolding as an early factor in PD.
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Excitatory synapses in the brain are often surrounded by nanoscopic astroglial processes that express high-affinity glutamate transporters at a high surface density. This ensures that the bulk of glutamate leaving the synaptic cleft is taken up for its subsequent metabolic conversion and replenishment in neurons. Furthermore, variations in the astroglial coverage of synapses can thus determine to what extent glutamate released into the synaptic cleft could activate its receptors outside the cleft.

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The correlation coefficient gauges linear association between two variables. However, interpreting its value depends on the question at hand. This article argues that relying on the correlation coefficient may be irrelevant for many neuroscience research tasks.

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Population behavior of signaling molecules on the cell surface is key to their adaptive function. Live imaging of proteins tagged with fluorescent molecules has been an essential tool in understanding this behavior. Typically, genetic or chemical tags are used to target molecules present throughout the cell, whereas antibody-based tags label the externally exposed molecular domains only.

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Brain ischemic stroke is among the leading causes of death and long-term disability. New treatments that alleviate brain cell damage until blood supply is restored are urgently required. The emerging focus of anti-stroke strategies has been on blood-brain-barrier permeable drugs that exhibit multiple sites of action.

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Polyetheretherketone (PEEK) is a high-performance semi-crystalline thermoplastic polymer with outstanding mechanical properties, high thermal stability, resistance to most common solvents, and good biocompatibility. A high temperature thermally induced phase separation technique was used to produce PEEK foams with controlled foam density from PEEK in 4-phenylphenol (4PPH) solutions. Physical and mechanical properties, foam and bulk density, surface area, and pore morphology of foamed PEEK were characterized and the role of PEEK concentration and cooling rate was investigated.

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The conservation of historical paper objects with high cultural value is an important societal task. Papers that have been severely damaged by fire, heat, and extinguishing water, are a particularly challenging case, because of the complexity and severity of damage patterns. In-depth analysis of fire-damaged papers, by means of examples from the catastrophic fire in a 17th-century German library, shows the changes, which proceeded from the margin to the center, to go beyond surface charring and formation of hydrophobic carbon-rich layers.

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Glutamatergic transmission prompts K efflux through postsynaptic NMDA receptors. The ensuing hotspot of extracellular K elevation depolarizes presynaptic terminal, boosting glutamate release, but whether this also affects glutamate uptake in local astroglia has remained an intriguing question. Here, we find that the pharmacological blockade, or conditional knockout, of postsynaptic NMDA receptors suppresses use-dependent increase in the amplitude and duration of the astrocytic glutamate transporter current (I ), whereas blocking astrocytic K channels prevents the duration increase only.

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The surface of astrocyte processes that often surround excitatory synapses is packed with high-affinity glutamate transporters, largely preventing extrasynaptic glutamate escape. The shape and prevalence of perisynaptic astroglia vary among brain regions, in some cases providing a complete isolation of synaptic connections from the surrounding tissue. The perception has been that the geometry of perisynaptic environment is therefore essential to preventing extrasynaptic glutamate escape.

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Human iPSC lines represent a powerful translational model of tauopathies. We have recently described a pathophysiological phenotype of neuronal excitability of human cells derived from the patients with familial frontotemporal dementia and parkinsonism (FTDP-17) caused by the MAPT 10+16 splice-site mutation. This mutation leads to the increased splicing of 4R tau isoforms.

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Behaviour of a mammal relies on the brain's excitatory circuits equipped with glutamatergic synapses. In most cases, glutamate escaping from the synaptic cleft is rapidly buffered and taken up by high-affinity transporters expressed by nearby perisynaptic astroglial processes (PAPs). The spatial relationship between glutamatergic synapses and PAPs thus plays a crucial role in understanding glutamate signalling actions, yet its intricate features can only be fully appreciated using methods that operate beyond the diffraction limit of light.

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Introduction: The second most common form of early-onset dementia-frontotemporal dementia (FTD)-is often characterized by the aggregation of the microtubule-associated protein tau. Here we studied the mechanism of tau-induced neuronal dysfunction in neurons with the FTD-related 10+16 MAPT mutation.

Methods: Live imaging, electrophysiology, and redox proteomics were used in 10+16 induced pluripotent stem cell-derived neurons and a model of tau spreading in primary cultures.

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Glutamate uptake by astroglial transporters confines excitatory transmission to the synaptic cleft. The efficiency of this mechanism depends on the transporter dynamics in the astrocyte membrane, which remains poorly understood. Here, we visualise the main glial glutamate transporter GLT1 by generating its pH-sensitive fluorescent analogue, GLT1-SEP.

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In obstacle-filled media, such as extracellular or intracellular lumen of brain tissue, effective ion-diffusion permeability is a key determinant of electrogenic reactions. Although this diffusion permeability is thought to depend entirely on structural features of the medium, such as porosity and tortuosity, brain tissue shows prominent nonohmic properties, the origins of which remain poorly understood. Here, we explore Monte Carlo simulations of ion diffusion in a space filled with overlapping spheres to predict that diffusion permeability of such media decreases with stronger external electric fields.

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A solid epoxy resin formulation containing 2.5 wt % carbon nanotubes is 3D printed into self-standing parts, which after thermal curing result in CNTs/epoxy nanocomposites with mechanical properties attractive for heavy-duty applications.

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Dendritic integration of synaptic inputs involves their increased electrotonic attenuation at distal dendrites, which can be counterbalanced by the increased synaptic receptor density. However, during network activity, the influence of individual synapses depends on their release fidelity, the dendritic distribution of which remains poorly understood. Here, we employed classical optical quantal analyses and a genetically encoded optical glutamate sensor in acute hippocampal slices of rats and mice to monitor glutamate release at CA3-CA1 synapses.

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