scholarly journals Cytotoxic edema: mechanisms of pathological cell swelling

2007 ◽  
Vol 22 (5) ◽  
pp. 1-9 ◽  
Author(s):  
Danny Liang ◽  
Sergei Bhatta ◽  
Volodymyr Gerzanich ◽  
J. Marc Simard
Keyword(s):  
Cerebral Edema ◽  
Molecular Mechanisms ◽  
Pathological Process ◽  
Cell Swelling ◽  
Cation Channels ◽  
Secondary Injury ◽  
Cytotoxic Edema ◽  
Pathological Conditions ◽  
The Brain

✓Cerebral edema is caused by a variety of pathological conditions that affect the brain. It is associated with two separate pathophysiological processes with distinct molecular and physiological antecedents: those related to cytotoxic (cellular) edema of neurons and astrocytes, and those related to transcapillary flux of Na+ and other ions, water, and serum macromolecules. In this review, the authors focus exclusively on the first of these two processes. Cytotoxic edema results from unchecked or uncompensated influx of cations, mainly Na+, through cation channels. The authors review the different cation channels that have been implicated in the formation of cytotoxic edema of astrocytes and neurons in different pathological states. A better understanding of these molecular mechanisms holds the promise of improved treatments of cerebral edema and of the secondary injury produced by this pathological process.

Molecular Mechanisms of Ischemic Cerebral Edema: Role of Electroneutral Ion Transport

Physiology ◽  
2009 ◽  
Vol 24 (4) ◽  
pp. 257-265 ◽  
Author(s):  
Kristopher T. Kahle ◽  
J. Marc Simard ◽  
Kevin J. Staley ◽  
Brian V. Nahed ◽  
Pamela S. Jones ◽  
...  
Keyword(s):  
Cerebral Edema ◽  
Molecular Mechanisms ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Ischemic Brain Injury ◽  
Edema Formation ◽  
Ischemic Brain ◽  
The Brain ◽  
Permeability Alterations

The brain achieves homeostasis of its intracellular and extracellular fluids by precisely regulating the transport of solute and water across its major cellular barriers: endothelia of the blood-brain barrier (BBB), choroid plexus epithelia, and neuroglial cell membranes. Cerebral edema, the pathological accumulation of fluid in the brain’s intracellular and extracellular spaces, is a major cause of morbidity and mortality following stroke and other forms of ischemic brain injury. Until recently, mechanisms of cerebral edema formation have been obscure; consequently, its treatment has been empiric and suboptimal. Here, we provide a paradigm for understanding ischemic cerebral edema, showing that its molecular pathogenesis is a complex yet step-wise process that results largely from impaired astrocytic cell volume regulation and permeability alterations in the cerebral microvasculature, both of which arise from pathological changes in the activities of specific ion channels and transporters. Recent data has implicated the bumetanide-sensitive NKCC1, an electroneutral cotransporter expressed in astrocytes and the BBB, in cerebral edema formation in several different rodent models of stroke. Pharmacological inhibition or genetic deficiency of NKCC1 decreases ischemia-induced cell swelling, BBB breakdown, cerebral edema, and neurotoxicity. Combination pharmacological strategies that include NKCC1 as a target might thus prove beneficial for the treatment of ischemic, and potentially other types of, cerebral edema.

scholarly journals Proopiomelanocortin, a polypeptide precursor with multiple functions: from physiology to pathological conditions

2003 ◽  
Vol 149 (2) ◽  
pp. 79-90 ◽  
Author(s):  
ML Raffin-Sanson ◽  
Y de Keyzer ◽  
X Bertagna
Keyword(s):  
Anterior Pituitary ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Single Gene ◽  
Local Production ◽  
Biological Functions ◽  
Multiple Functions ◽  
Pathological Conditions ◽  
Recent Developments ◽  
The Brain

Proopiomelanocortin (POMC) is the polypeptide precursor of ACTH. First discovered in anterior pituitary corticotroph cells, it has more recently been revealed to have many other physiological aspects. The fine molecular mechanisms of ACTH biosynthesis show that ACTH is but one piece of a puzzle which contains many other peptides. Present in various tIssues, among which are pituitary, hypothalamus, central nervous system and skin, POMC undergoes extensive post-translational processing. This processing is tIssue-specific and generates, depending on the case, various sets of peptides involved in completely diverse biological functions. POMC expressed in corticotroph cells of the pituitary is necessary for adrenal function. Recent developments have shown that POMC-expressing neurons in the brain play a major role in the control of pain and energy homeostasis. Local production of POMC-derived peptides in skin may influence melanogenesis. A still unknown function in the placenta is likely.POMC has become a paradigmatic polypeptide precursor model illustrating the variable roles of a single gene and its various products in different localities.

scholarly journals Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

2013 ◽  
Vol 30 (11) ◽  
pp. 920-937 ◽  
Author(s):  
Patrick M. Kochanek ◽  
C. Edward Dixon ◽  
David K. Shellington ◽  
Samuel S. Shin ◽  
Hülya Bayır ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Secondary Injury ◽  
Injury And Repair ◽  
The Brain

scholarly journals Neural stem cells-from quiescence to differentiation and potential clinical uses

2021 ◽  
Vol 4 (1) ◽  
pp. 23-41
Author(s):  
Alexandra-Elena Dobranici ◽  
Sorina Dinescu ◽  
Marieta Costache
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Molecular Mechanisms ◽  
Adult Brain ◽  
Quiescent State ◽  
Multipotent Stem Cells ◽  
Pathological Conditions ◽  
Mature Neurons ◽  
Direct Cell ◽  
The Brain

Specialised cells of the brain are generated from a population of multipotent stem cells found in the forming embryo and adult brain after birth, called neural stem cells. They reside in specific niches, usually in a quiescent, non-proliferating state that maintains their reservoir. Neural stem cells are kept inactive by various cues such as direct cell-cell contacts with neighbouring cells or by soluble molecules that trigger intracellular responses. They are activated in response to injuries, physical exercise, or hypoxia condition, through stimulation of signaling pathways that are usually correlated with increased proliferation and survival. Moreover, mature neurons play essential role in regulating the balance between active and quiescent state by realising inhibitory or activating neurotransmitters. Understanding molecular mechanisms underlying neuronal differentiation is of great importance in elucidating pathological conditions of the brain and treating neurodegenerative disorders that until now have no efficient therapies.

Consequences of Anoxia and Ischemia to the Brain

2019 ◽  
pp. 86-91
Author(s):  
Jennifer E. Fugate
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Cerebral Edema ◽  
Secondary Injury ◽  
Neurologic Manifestations ◽  
Ischemic Brain ◽  
Electrolyte Disturbances ◽  
The Central Nervous System ◽  
The Brain

Systemic illness can have an abrupt and sometimes profound effect on the central nervous system. Organ failure and acute electrolyte disturbances may cause neurologic manifestations that are often accompanied by a decline in consciousness. Secondary injury is characterized by demyelination, cerebral edema, and anoxic-ischemic brain injury.

CLINICAL AND NEUROLOGICAL FEATURES OF TRAUMATIC BRAIN DISEASE DURING THE STAGES OF REHABILITATION

2020 ◽  
Vol 3 (1) ◽  
pp. 51-53
Author(s):  
Rano Azizova ◽  
◽  
Umida Shamsiyeva ◽  
Mirzohid Turabbayev ◽  
Begzod Jorayev ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Pathological Process ◽  
Brain Disease ◽  
Clinical Forms ◽  
Neurological Features ◽  
Mechanisms Of Development ◽  
The Brain

Traumatic brain disease (TBHD) is a pathological process triggered by the damaging effect of mechanical energy on the brain and is characterized — with a variety of clinical forms — by the unity of etiology, pathogenetic and sanogenetic mechanisms of development and outcomes.

scholarly journals Sublethal Exposure Effects of the Neonicotinoid Clothianidin Strongly Modify the Brain Transcriptome and Proteome in the Male Moth Agrotis ipsilon

Insects ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 152
Author(s):  
Camille Meslin ◽  
Françoise Bozzolan ◽  
Virginie Braman ◽  
Solenne Chardonnet ◽  
Cédric Pionneau ◽  
...  
Keyword(s):  
Sex Pheromone ◽  
Molecular Mechanisms ◽  
Insect Pest ◽  
Agrotis Ipsilon ◽  
Positive Effects ◽  
Male Moth ◽  
Hormetic Effect ◽  
Pest Insects ◽  
Neuronal Processes ◽  
The Brain

Insect pest management relies mainly on neurotoxic insecticides, including neonicotinoids such as clothianidin. The residual accumulation of low concentrations of these insecticides can have positive effects on target pest insects by enhancing various life traits. Because pest insects often rely on sex pheromones for reproduction and olfactory synaptic transmission is cholinergic, neonicotinoid residues could indeed modify chemical communication. We recently showed that treatments with low doses of clothianidin could induce hormetic effects on behavioral and neuronal sex pheromone responses in the male moth, Agrotis ipsilon. In this study, we used high-throughput RNAseq and proteomic analyses from brains of A. ipsilon males that were intoxicated with a low dose of clothianidin to investigate the molecular mechanisms leading to the observed hormetic effect. Our results showed that clothianidin induced significant changes in transcript levels and protein quantity in the brain of treated moths: 1229 genes and 49 proteins were differentially expressed upon clothianidin exposure. In particular, our analyses highlighted a regulation in numerous enzymes as a possible detoxification response to the insecticide and also numerous changes in neuronal processes, which could act as a form of acclimatization to the insecticide-contaminated environment, both leading to enhanced neuronal and behavioral responses to sex pheromone.

scholarly journals DNA Methylation Profiles of Tph1A and BDNF in Gut and Brain of L. Rhamnosus-Treated Zebrafish

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 142
Author(s):  
Mariella Cuomo ◽  
Luca Borrelli ◽  
Rosa Della Monica ◽  
Lorena Coretti ◽  
Giulia De Riso ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Molecular Mechanisms ◽  
The Past ◽  
Targeted Analysis ◽  
Lack Of Information ◽  
High Resolution Power ◽  
Resolution Level ◽  
Health And Disease ◽  
High Doses ◽  
The Brain

The bidirectional microbiota–gut–brain axis has raised increasing interest over the past years in the context of health and disease, but there is a lack of information on molecular mechanisms underlying this connection. We hypothesized that change in microbiota composition may affect brain epigenetics leading to long-lasting effects on specific brain gene regulation. To test this hypothesis, we used Zebrafish (Danio Rerio) as a model system. As previously shown, treatment with high doses of probiotics can modulate behavior in Zebrafish, causing significant changes in the expression of some brain-relevant genes, such as BDNF and Tph1A. Using an ultra-deep targeted analysis, we investigated the methylation state of the BDNF and Tph1A promoter region in the brain and gut of probiotic-treated and untreated Zebrafishes. Thanks to the high resolution power of our analysis, we evaluated cell-to-cell methylation differences. At this resolution level, we found slight DNA methylation changes in probiotic-treated samples, likely related to a subgroup of brain and gut cells, and that specific DNA methylation signatures significantly correlated with specific behavioral scores.

scholarly journals Molecular mechanisms of metabotropic GABAB receptor function

2021 ◽  
Vol 7 (22) ◽  
pp. eabg3362
Author(s):  
Hamidreza Shaye ◽  
Benjamin Stauch ◽  
Cornelius Gati ◽  
Vadim Cherezov
Keyword(s):  
G Protein ◽  
Molecular Mechanisms ◽  
Gabab Receptor ◽  
Neurological Diseases ◽  
Activation Mechanism ◽  
Allosteric Modulators ◽  
Inhibitory Neurotransmitter ◽  
Therapeutic Drugs ◽  
G Protein Coupled ◽  
The Brain

Metabotropic γ-aminobutyric acid G protein–coupled receptors (GABAB) represent one of the two main types of inhibitory neurotransmitter receptors in the brain. These receptors act both pre- and postsynaptically by modulating the transmission of neuronal signals and are involved in a range of neurological diseases, from alcohol addiction to epilepsy. A series of recent cryo-EM studies revealed critical details of the activation mechanism of GABAB. Structures are now available for the receptor bound to ligands with different modes of action, including antagonists, agonists, and positive allosteric modulators, and captured in different conformational states from the inactive apo to the fully active state bound to a G protein. These discoveries provide comprehensive insights into the activation of the GABAB receptor, which not only broaden our understanding of its structure, pharmacology, and physiological effects but also will ultimately facilitate the discovery of new therapeutic drugs and neuromodulators.

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