BDNF signaling requires Matrix Metalloproteinase-9 during structural synaptic plasticity.

Synaptic plasticity underlies learning and memory processes as well as contributes, in its aberrant form, to neuropsychiatric disorders. One of its major forms is structural long-term potentiation (sLTP), an activity-dependent growth of dendritic spines that harbor excitatory synapses. The process depends on the release of brain-derived neurotrophic factor (BDNF), and activation of its receptor, TrkB.

Impact of elastic substrate on the dynamic heterogeneity of WC256 Walker carcinosarcoma cells.

Cellular heterogeneity is a phenomenon in which cell populations are composed of subpopulations that vary in their behavior. Heterogeneity is particularly pronounced in cancer cells and can affect the efficacy of oncological therapies. Previous studies have considered heterogeneity dynamics to be indicative of evolutionary changes within subpopulations; however, these studies do not consider the short-time morphological plasticity of cells.

Morphomigrational description as a new approach connecting cell's migration with its morphology.

The examination of morphology and migration of cells plays substantial role in understanding the cellular behaviour, being described by plethora of quantitative parameters and models. These descriptions, however, treat cell migration and morphology as independent properties of temporal cell state, while not taking into account their strong interdependence in adherent cells. Here we present the new and simple mathematical parameter called signed morphomigrational angle (sMM angle) that links cell geometry with translocation of cell centroid, considering them as one morphomigrational behaviour.

Phosphorylation of PSD-95 at serine 73 in dCA1 is required for extinction of contextual fear.

The updating of contextual memories is essential for survival in a changing environment. Accumulating data indicate that the dorsal CA1 area (dCA1) contributes to this process. However, the cellular and molecular mechanisms of contextual fear memory updating remain poorly understood.

Altered trafficking of miRNAs at mitochondria modulates mitochondrial functions and cell death in brain ischemia.

Stroke is one of the major causes of death and disabilities worldwide. The rapid induction of cell death by necrosis and apoptosis is observed at the ischemic core, while long lasting apoptosis and brain inflammation continue in the penumbra. The emerging evidence suggests a critical role of mitochondria in acute and chronic inflammation and cell death.

Emerging Molecular Targets for Anti-Epileptogenic and Epilepsy Modifying Drugs.

The pharmacological treatment of epilepsy is purely symptomatic. Despite many decades of intensive research, causal treatment of this common neurologic disorder is still unavailable. Nevertheless, it is expected that advances in modern neuroscience and molecular biology tools, as well as improved animal models may accelerate designing antiepileptogenic and epilepsy-modifying drugs.

3dSpAn: An interactive software for 3D segmentation and analysis of dendritic spines.

Three-dimensional segmentation and analysis of dendritic spine morphology involve two major challenges: 1) how to segment individual spines from the dendrites and 2) how to quantitatively assess the morphology of individual spines. To address these two issues, we developed software called 3dSpAn (3-dimensional Spine Analysis), based on implementing a previously published method, 3D multi-scale opening algorithm in shared intensity space. 3dSpAn consists of four modules: a) Preprocessing and Region of Interest (ROI) selection, b) Intensity thresholding and seed selection, c) Multi-scale segmentation, and d) Quantitative morphological feature extraction.

RFCM-PALM: In-Silico Prediction of S-Palmitoylation Sites in the Synaptic Proteins for Male/Female Mouse Data.

S-palmitoylation is a reversible covalent post-translational modification of cysteine thiol side chain by palmitic acid. S-palmitoylation plays a critical role in a variety of biological processes and is engaged in several human diseases. Therefore, identifying specific sites of this modification is crucial for understanding their functional consequences in physiology and pathology.

Exocytosis in Astrocytes.

Until recently, astrocytes were thought to be a part of a simple "brain glue" providing only a supporting role for neurons. However, the discoveries of the last two decades have proven astrocytes to be dynamic partners participating in brain metabolism and actively influencing communication between neurons. The means of astrocyte-neuron communication are diverse, although regulated exocytosis has received the most attention but also caused the most debate.

Two weeks of moderate intensity locomotor training increased corticosterone concentrations but did not alter the number of adropin-immunoreactive cells in the hippocampus of diabetic type 2 and control rats.

Adropin (ADR) plays a role in metabolism regulation and its alterations in obesity and diabetes have been found. Treatment with ADR was beneficial in metabolic diseases, and physical exercise increased ADR concentrations in obese patients. However, data on the distribution of ADR in the brain are sparse.

Development of novel derivatives of stilbene and macrocyclic compounds as potent of anti-microtubule factors.

Microtubules (composed of α- and β-tubulin heterodimers) ubiquitous cellular polymers are important components of the cytoskeleton and play diverse roles within the cell, such as maintenance of cell structure, protein trafficking or chromosomal segregation during cell division. The polymers of tubulin play a pivotal role in mitosis and are regarded as an excellent target for chemotherapeutic agents to treat cancer. This review presents a brief overview of the synthesis and mechanism of action of new compounds targeting the dynamic of microtubule - tubulin polymerization/depolymerization.

Sequential changes in histone modifications shape transcriptional responses underlying microglia polarization by glioma.

Microglia, resident myeloid cells of the central nervous system (CNS), act as immune sentinels that contribute to maintenance of physiological homeostasis and respond to any perturbation in CNS. Microglia could be polarized by various stimuli to perform dedicated functions and instigate inflammatory or pro-regenerative responses. Microglia and peripheral macrophages accumulate in glioblastomas (GBMs), malignant brain tumors, but instead of initiating antitumor responses, these cells are polarized to the pro-invasive and immunosuppressive phenotype which persists for a long time and contributes to a "cold" immune microenvironment of GBMs.

Insight into the Structural Dynamics of the Lysenin During Prepore-to-Pore Transition Using Hydrogen-Deuterium Exchange Mass Spectrometry.

Lysenin is a pore-forming toxin of the aerolysin family, which is derived from coelomic fluid of the earthworm . Upon binding to sphingomyelin (SM)-containing membranes, lysenin undergoes a series of structural changes promoting the conversion of water-soluble monomers into oligomers, leading to its insertion into the membrane and the formation of a lytic β-barrel pore. The soluble monomer and transmembrane pore structures were recently described, but the underlying structural details of oligomerization remain unclear.

Search for novel STAT3-dependent genes reveals SERPINA3 as a new STAT3 target that regulates invasion of human melanoma cells.

Transcription factor signal transducer and activator of transcription 3 (STAT3) is constitutively activated in many cancers and promotes uncontrolled tumor growth and progression through multiple mechanisms. Compelling evidence shows tissue and cell-specific sets of STAT3 targets. Transcriptional targets of STAT3 in melanoma cells are largely unknown.

Prophylactic Ketamine Treatment Promotes Resilience to Chronic Stress and Accelerates Recovery: Correlation with Changes in Synaptic Plasticity in the CA3 Subregion of the Hippocampus.

Ketamine is an -methyl-d-aspartate receptor antagonist that has gained wide attention as a potent antidepressant. It has also been recently reported to have prophylactic effects in animal models of depression and anxiety. Alterations of neuroplasticity in different brain regions; such as the hippocampus; prefrontal cortex; and amygdala; are a hallmark of stress-related disorders; and such changes may endure beyond the treatment of symptoms.

Knockdown of STAT3 targets a subpopulation of invasive melanoma stem-like cells.

Transcription factor signal transducer and activator of transcription 3 (STAT3) is constitutively activated in many cancers, including melanomas. Active, phosphorylated STAT3 contributes to tumor growth and formation of the immunosuppressive tumor microenvironment. Recent evidence suggests an important role of STAT3 in self-renewal of cancer stem-like cells (CSCs).

Neuronal plasticity affects correlation between the size of dendritic spine and its postsynaptic density.

Structural plasticity of dendritic spines is thought to underlie memory formation. Size of a dendritic spine is considered proportional to the size of its postsynaptic density (PSD), number of glutamate receptors and synaptic strength. However, whether this correlation is true for all dendritic spine volumes, and remains stable during synaptic plasticity, is largely unknown.

Histone deacetylase inhibitors exert anti-tumor effects on human adherent and stem-like glioma cells.

Background: The diagnosis of glioblastoma (GBM), a most aggressive primary brain tumor with a median survival of 14.6 months, carries a dismal prognosis. GBMs are characterized by numerous genetic and epigenetic alterations, affecting patient survival and treatment response.

Dissecting functional phenotypes of microglia and macrophages in the rat brain after transient cerebral ischemia.

Ischemic brain injury causes local inflammation, which involves activation of resident microglia, leukocyte, and monocyte infiltration. Involvement of peripheral immune cells in ischemia-induced damage and repair is debatable. Using flow cytometry, gene expression profiling, and immunocytochemistry, we show that microglia predominate in the ischemic brain and express inflammation mediators at Day 1 after transient middle cerebral artery occlusion (MCAo) in rats.

Fine-tuning of the stability of β-strands by Y181 in perfringolysin O directs the prepore to pore transition.

Perfringolysin O (PFO) is a toxic protein that forms β-barrel transmembrane pores upon binding to cholesterol-containing membranes. The formation of lytic pores requires conformational changes in PFO that lead to the conversion of water-soluble monomers into membrane-bound oligomers. Although the general outline of stepwise pore formation has been established, the underlying mechanistic details await clarification.

miR-124-3p is a chronic regulator of gene expression after brain injury.

Traumatic brain injury (TBI) initiates molecular and cellular pathologies that underlie post-injury morbidities, including hippocampus-related memory decline and epileptogenesis. Non-coding small RNAs are master regulators of gene expression with the potential to affect multiple molecular pathways. To evaluate whether hippocampal gene expression networks are chronically regulated by microRNAs after TBI, we sampled the dentate gyrus of rats with severe TBI induced by lateral fluid-percussion injury 3 months earlier.

Generation of silent synapses in dentate gyrus correlates with development of alcohol addiction.

The brain circuits and synaptic processes that underlie alcohol addiction are currently the subject of intensive research. Here we focus on hippocampal circuitry and show that chemogenetic inhibition of dentate gyrus (DG) during presentation of alcohol-associated cues has long-lasting effects on mice behavior. DG inhibition enhances alcohol seeking and drinking, suggesting that DG regulates addiction-related behaviors.