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Spreading depolarization

Krzysztof Kucharz, Martin Lauritzen
Cortical spreading depolarization waves, the cause underlying migraine aura, are also the markers and mechanism of pathology in the acutely injured human brain. Propagation of spreading depolarization wave uniquely depends on the interaction between presynaptic and postsynaptic glutamate N-methyl-d-aspartate receptors (NMDARs). In the normally perfused brain, even a single wave causes a massive depolarization of neurons and glia, which results in transient loss of neuronal function and depression of the ongoing electrocorticographic activity...
March 12, 2018: Brain: a Journal of Neurology
Néstor Wainsztein, Federico Rodríguez Lucci
Spreading depolarization in cerebral cortex is associated with swelling of neurons, distortion of dendritic spines, massive ion translocation with a large change of the slow electrical potential, and silencing of brain electrical activity. The term spreading depression represents a wave of spontaneous activity of the electrocorticogram that propagates through contiguous cerebral gray matter at a characteristic velocity. Spreading depression is a consequence of cortical spreading depolarization. Therefore, spreading depolarization is not always accompanied by spreading depression and the terms are not synonymous...
April 2018: Neurosurgery Clinics of North America
Shasha Chen, Christopher Lotz, Norbert Roewer, Jens-Albert Broscheit
Volatile anesthetic-induced preconditioning (APC) has shown to have cardiac and cerebral protective properties in both pre-clinical models and clinical trials. Interestingly, accumulating evidences demonstrate that, except from some specific characters, the underlying molecular mechanisms of APC-induced protective effects in myocytes and neurons are very similar; they share several major intracellular signaling pathways, including mediating mitochondrial function, release of inflammatory cytokines and cell apoptosis...
February 20, 2018: European Journal of Medical Research
Olga Cozzolino, Maria Marchese, Francesco Trovato, Enrico Pracucci, Gian Michele Ratto, Maria Gabriella Buzzi, Federico Sicca, Filippo M Santorelli
Spreading depression (SD) is a neurophysiological phenomenon characterized by abrupt changes in intracellular ion gradients and sustained depolarization of neurons. It leads to loss of electrical activity, changes in the synaptic architecture, and an altered vascular response. Although SD is often described as a unique phenomenon with homogeneous characteristics, it may be strongly affected by the particular triggering event and by genetic background. Furthermore, SD may contribute differently to the pathogenesis of widely heterogeneous clinical conditions...
2018: Frontiers in Neurology
Jaime L Hook, Mohammad N Islam, Dane Parker, Alice S Prince, Sunita Bhattacharya, Jahar Bhattacharya
Infection by Staphylococcus aureus strain USA300 causes tissue injury, multiorgan failure, and high mortality. However, the mechanisms by which the bacteria adhere to, then stabilize on, mucosal surfaces before causing injury remain unclear. We addressed these issues through the first real-time determinations of USA300-alveolar interactions in live lungs. We found that within minutes, inhaled USA300 established stable, self-associated microaggregates in niches at curved, but not at flat, regions of the alveolar wall...
February 12, 2018: Journal of Clinical Investigation
David Y Chung, Homa Sadeghian, Tao Qin, Sevda Lule, Hang Lee, Fahri Karakaya, Stacy Goins, Fumiaki Oka, Mohammad A Yaseen, Thijs Houben, Else A Tolner, Arn M J M van den Maagdenberg, Michael J Whalen, Sava Sakadžic, Cenk Ayata
Cortical spreading depolarization (SD) is the electrophysiological event underlying migraine aura, and a critical contributor to secondary damage after brain injury. Experimental models of SD have been used for decades in migraine and brain injury research; however, they are highly invasive and often cause primary tissue injury, diminishing their translational value. Here we present a non-invasive method to trigger SDs using light-induced depolarization in transgenic mice expressing channelrhodopsin-2 in neurons (Thy1-ChR2-YFP)...
February 7, 2018: Cerebral Cortex
Jeannette Hofmeijer, C R van Kaam, Babette van de Werff, Sarah E Vermeer, Marleen C Tjepkema-Cloostermans, Michel J A M van Putten
Introduction: There is strong evidence suggesting detrimental effects of cortical spreading depolarization (CSD) in patients with acute ischemic stroke and severe traumatic brain injury. Previous studies implicated scalp electroencephalography (EEG) features to be correlates of CSD based on retrospective analysis of EEG epochs after having detected "CSD" in time aligned electrocorticography. We studied the feasibility of CSD detection in a prospective cohort study with continuous EEG in 18 patients with acute ischemic stroke and 18 with acute severe traumatic brain injury...
2018: Frontiers in Neurology
Maosen Wang, Yi He, Terrence J Sejnowski, Xin Yu
Astrocytic Ca2+-mediated gliovascular interactions regulate the neurovascular network in situ and in vivo. However, it is difficult to measure directly both the astrocytic activity and fMRI to relate the various forms of blood-oxygen-level-dependent (BOLD) signaling to brain states under normal and pathological conditions. In this study, fMRI and GCaMP-mediated Ca2+ optical fiber recordings revealed distinct evoked astrocytic Ca2+ signals that were coupled with positive BOLD signals and intrinsic astrocytic Ca2+ signals that were coupled with negative BOLD signals...
January 30, 2018: Proceedings of the National Academy of Sciences of the United States of America
Micol E Fiori, Lidia Villanova, Chiara Barbini, Maria Laura De Angelis, Ruggero De Maria
Treatment of lung cancer is an unmet need as it accounts for the majority of cancer deaths worldwide. The development of new therapies urges the identification of potential targets. MicroRNAs' expression is often deregulated in cancer and their modulation has been proposed as a successful strategy to interfere with tumor cell growth and spread. We recently reported on an unbiased high-content approach to identify miRNAs regulating cell proliferation and tumorigenesis in non-small cell lung cancer (NSCLC). Here we studied the oncogenic role of miR-663 in NSCLC biology and analyzed the therapeutic potential of miR-663 targeting...
January 19, 2018: Cell Death & Disease
A Yu Verisokin, D V Verveyko, D E Postnov
Cortical spreading depression (CSD) along with migraine waves and spreading depolarization events with stroke or injures are the front-line examples of extreme physiological behaviors of the brain cortex which manifest themselves via the onset and spreading of localized areas of neuronal hyperactivity followed by their depression. While much is known about the physiological pathways involved, the dynamical mechanisms of the formation and evolution of complex spatiotemporal patterns during CSD are still poorly understood, in spite of the number of modeling studies that have been already performed...
December 2017: Physical Review. E
Jens P Dreier, Sebastian Major, Brandon Foreman, Maren K L Winkler, Eun-Jeung Kang, Denny Milakara, Coline L Lemale, Vince DiNapoli, Jason M Hinzman, Johannes Woitzik, Norberto Andaluz, Andrew Carlson, Jed A Hartings
OBJECTIVE: Restoring the circulation is the primary goal in emergency treatment of cerebral ischemia. However, better understanding of how the brain responds to energy depletion could inform the time available for resuscitation until irreversible damage and advance development of interventions that prolong this span. Experimentally, injury to central neurons begins only with anoxic depolarization. This potentially reversible, spreading wave typically starts 2-5 min after the onset of severe ischemia, marking the onset of a toxic intraneuronal change that eventually results in irreversible injury...
January 13, 2018: Annals of Neurology
Philippe Jean, David Lopez de la Morena, Susann Michanski, Lina María Jaime Tobón, Rituparna Chakrabarti, Maria Magdalena Picher, Jakob Neef, SangYong Jung, Mehmet Gültas, Stephan Maxeiner, Andreas Neef, Carolin Wichmann, Nicola Strenzke, Chad Grabner, Tobias Moser
We studied the role of the synaptic ribbon for sound encoding at the synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in mice lacking RIBEYE (RBEKO/KO). Electron and immunofluorescence microscopy revealed a lack of synaptic ribbons and an assembly of several small active zones (AZs) at each synaptic contact. Spontaneous and sound-evoked firing rates of SGNs and their compound action potential were reduced, indicating impaired transmission at ribbonless IHC-SGN synapses. The temporal precision of sound encoding was impaired and the recovery of SGN-firing from adaptation indicated slowed synaptic vesicle (SV) replenishment...
January 12, 2018: ELife
Jie Xin Tong, Rajesh Chandramohanadas, Kevin Shyong-Wei Tan
Plasmodium falciparum infections leading to malaria have severe clinical manifestations and high mortality rates. Chloroquine (CQ), a former mainstay of malaria chemotherapy, has been rendered ineffective due to the emergence of wide-spread resistance. Recent studies, however, have unveiled a novel mode of action in which low micromolar levels of CQ permeabilized the parasite's digestive vacuole (DV) membrane, leading to calcium efflux, mitochondrial depolarization and DNA degradation. These phenotypes implicate the DV as an alternative target of CQ and suggests that DV disruption is an attractive target for exploitation through the screening for DV-disruptive antimalarials...
January 8, 2018: Antimicrobial Agents and Chemotherapy
Francesca Eroli, Inge C M Loonen, Arn M J M van den Maagdenberg, Else A Tolner, Andrea Nistri
Endocannabinoids are suggested to control pain, even though their clinical use is not fully validated and the underlying mechanisms are incompletely understood. To clarify the targets of endocannabinoid actions, we studied how activation of the endocannabinoid CB1 receptor (CB1R) affects neuronal responses in two in vitro preparations of rodents, namely the trigeminal sensory ganglion (TG) in culture and a coronal slice of the cerebral cortex. On TG small-medium size neurons, we tested whether submicromolar concentrations of the endogenous CB1R agonist anandamide (AEA) modulated inhibitory GABAA receptors and excitatory ATP-gated P2X3 receptors...
March 15, 2018: Neuropharmacology
Cameron Conte, Ray Lee, Monica Sarkar, David Terman
A detailed biophysical model for a neuron/astrocyte network is developed in order to explore mechanisms responsible for the initiation and propagation of recurrent cortical spreading depolarizations. The model incorporates biophysical processes not considered in the earlier models. This includes a model for the Na+ -glutamate transporter, which allows for a detailed description of reverse glutamate uptake. In particular, we consider the specific roles of elevated extracellular glutamate and K+ in the initiation, propagation and recurrence of spreading depolarizations...
December 5, 2017: Journal of Computational Neuroscience
Satoko Kawauchi, Izumi Nishidate, Hiroshi Nawashiro, Shunichi Sato
In ischemic stroke research, a better understanding of the pathophysiology and development of neuroprotection methods are crucial, for which in vivo imaging to monitor spreading depolarizations (SDs) and evolution of tissue damage is desired. Since these events are accompanied by cellular morphological changes, light-scattering signals, which are sensitive to cellular and subcellular morphology, can be used for monitoring them. In this study, we performed transcranial imaging of near-infrared (NIR) diffuse reflectance at ∼800 nm, which sensitively reflects light-scattering change, and examined how NIR reflectance is correlated with simultaneously measured cerebral blood flow (CBF) for a rat middle cerebral artery occlusion (MCAO) model...
November 18, 2017: Journal of Neuroscience Research
Joseph R Geraghty, Fernando D Testai
PURPOSE OF REVIEW: Delayed cerebral ischemia (DCI) is common after subarachnoid hemorrhage (SAH) and represents a significant cause of poor functional outcome. DCI was mainly thought to be caused by cerebral vasospasm; however, recent clinical trials have been unable to confirm this hypothesis. Studies in humans and animal models have since supported the notion of a multifactorial pathophysiology of DCI. This review summarizes some of the main mechanisms under investigation including cerebral vascular dysregulation, microthrombosis, cortical spreading depolarizations, and neuroinflammation...
October 23, 2017: Current Atherosclerosis Reports
Hisao Yamamura, Keisuke Kawasaki, Sou Inagaki, Yoshiaki Suzuki, Yuji Imaizumi
Spatiotemporal changes in cytosolic Ca(2+) concentration ([Ca(2+)]c) trigger a number of physiological functions in smooth muscle cells (SMCs). We previously imaged Ca(2+)-induced Ca(2+) release following membrane depolarization as local Ca(2+) transients, Ca(2+) hotspots, in subplasmalemmal regions. In this study, the physiological significance of mitochondria on local Ca(2+) signaling was examined. Cytosolic and mitochondrial Ca(2+) images following depolarization or action potentials were recorded in single SMCs from the guinea pig urinary bladder using a fast-scanning confocal fluorescent microscope...
October 18, 2017: American Journal of Physiology. Cell Physiology
Miyuki Unekawa, Keiko Ikeda, Yutaka Tomita, Kiyoshi Kawakami, Norihiro Suzuki
Background Patients with familial hemiplegic migraine type 2 (FHM2) have a mutated ATP1A2 gene (encoding Na+,K+-ATPase α2 subunit) and show prolonged migraine aura. Cortical spreading depression (CSD), which involves mass depolarization of neurons and astrocytes that propagates slowly through the gray matter, is profoundly related to aura. Methods In two types of Atp1a2-defective heterozygous mice, Atp1a2tm1Kwk (C-KO) and Atp1a2tm2Kwk (N-KO), the sensitivity and responsiveness to CSD were examined under urethane anesthesia...
January 1, 2017: Cephalalgia: An International Journal of Headache
Niklas Hübel, Mahshid S Hosseini-Zare, Jokūbas Žiburkus, Ghanim Ullah
Simultaneous changes in ion concentrations, glutamate, and cell volume together with exchange of matter between cell network and vasculature are ubiquitous in numerous brain pathologies. A complete understanding of pathological conditions as well as normal brain function, therefore, hinges on elucidating the molecular and cellular pathways involved in these mostly interdependent variations. In this paper, we develop the first computational framework that combines the Hodgkin-Huxley type spiking dynamics, dynamic ion concentrations and glutamate homeostasis, neuronal and astroglial volume changes, and ion exchange with vasculature into a comprehensive model to elucidate the role of glutamate uptake in the dynamics of spreading depolarization (SD)-the electrophysiological event underlying numerous pathologies including migraine, ischemic stroke, aneurysmal subarachnoid hemorrhage, intracerebral hematoma, and trauma...
October 2017: PLoS Computational Biology
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