scholarly journals Noradrenergic Agonists and Antagonists Influence Migration of Cortical Spreading Depression in Rat—a Possible Mechanism of Migraine Prophylaxis and Prevention of Postischemic Neuronal Damage

2005 ◽  
Vol 25 (9) ◽  
pp. 1225-1235 ◽  
Author(s):  
Frank Richter ◽  
Oskar Mikulik ◽  
Andrea Ebersberger ◽  
Hans-Georg Schaible
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Regional Cerebral Blood ◽  
Adrenergic Agonist ◽  
Adult Rats ◽  
Arterial Blood ◽  
Β Blocker ◽  
Β Receptor ◽  
Focal Brain Ischemia

Cortical spreading depression (CSD) is thought to be a neuronal mechanism that expands the penumbra zone after focal brain ischemia and that causes migraine aura. Both adrenergic agonists and antagonists significantly influence the size of the penumbra zone and decline the frequency of migraine. To study whether these compounds act by influencing CSD, we applied different drugs topically to an area of the exposed cortex of anesthetized adult rats and observed the migration of CSD-related DC potential deflections across the treated area. The adrenergic agonist norepinephrine (1 mmol/L) and the α2-agonist clonidine (0.56 mmol/L) blocked reversibly the migration of CSD. The β-blocker propranolol (250 μmol/L to 1 mmol/L) dose-dependently diminished migration velocity or even blocked migration of CSD. The CSD blockade by the α2-antagonist yohimbine (1.75 mmol/L) was because of its action on inhibitory 5-HT1A receptors. None of the substances in the concentrations used had influence on regional cerebral blood flow or on systemic arterial blood pressure. The data suggest that the interference of these compounds with CSD may contribute to their beneficial therapeutic effect. The effect of β-receptor antagonists in human migraine needs further exploration, since these drugs also work in migraine without aura.

scholarly journals Cortical Spreading Depression Shifts Cell Fate Determination of Progenitor Cells in the Adult Cortex

2012 ◽  
Vol 32 (10) ◽  
pp. 1879-1887 ◽  
Author(s):  
Yasuhisa Tamura ◽  
Asami Eguchi ◽  
Guanghua Jin ◽  
Mustafa M Sami ◽  
Yosky Kataoka
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Immunohistochemical Analysis ◽  
Adult Rats ◽  
Brain Functions ◽  
Ng2 Cells ◽  
Neuronal Functions

Cortical spreading depression (SD) is propagating neuronal and glial depolarization and is thought to underly the pathophysiology of migraine. We have reported that cortical SD facilitates the proliferative activity of NG2-containing progenitor cells (NG2 cells) that give rise to oligodendrocytes and immature neurons under the physiological conditions in the adult mammalian cortex. Astrocytes have an important role in the maintenance of neuronal functions and alleviate neuronal damage after intense neuronal excitation, including SD and seizures. We here investigated whether SD promotes astrocyte generation from NG2 cells following SD stimuli. Spreading depression was induced by epidural application of 1 mol/L KCl solution in adult rats. We investigated the cell fate of NG2 cells following SD-induced proliferation using 5′-bromodeoxyuridine labeling and immunohistochemical analysis. Newly generated astrocytes were observed only in the SD-stimulated cortex, but not in the contralateral cortex or in normal cortex. The astrocytes were generated from proliferating NG2 cells. Astrogenesis depended on the number of SD stimuli, and was accompanied by suppression of oligodendrogenesis. These observations indicate that the cell fate of NG2 cells was shifted from oligodendrocytes to astrocytes depending on SD stimuli, suggesting activity-dependent tissue remodeling for maintenance of brain functions.

scholarly journals Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

2010 ◽  
Vol 31 (1) ◽  
pp. 17-35 ◽  
Author(s):  
Martin Lauritzen ◽  
Jens Peter Dreier ◽  
Martin Fabricius ◽  
Jed A Hartings ◽  
Rudolf Graf ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Disorders ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Ion Homeostasis ◽  
Large Body ◽  
Treatment Strategies ◽  
Pathophysiological Mechanism

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

scholarly journals Acute tryptophan administration impairs cortical spreading depression propagation in REM sleep deprived and non-deprived adult rats.

2009 ◽  
Vol 2 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Euclides Mauricio Trindade-Filho ◽  
Carlos Augusto Carvalho de Vasconcelos ◽  
Rubem Carlos Araújo Guedes
Keyword(s):  
Rem Sleep ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Adult Rats

scholarly journals Cerebral cortex does not modulate “regulated” decrease in core temperature during hypoxemia in rats

1998 ◽  
Vol 274 (4) ◽  
pp. R1158-R1161
Author(s):  
Evvi-Lynn M. Rollins ◽  
James E. Fewell
Keyword(s):  
Cerebral Cortex ◽  
Core Temperature ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Temperature Response ◽  
Sprague Dawley ◽  
Adult Rats ◽  
The Core ◽  
Sprague Dawley Rats ◽  
Before And After

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.

Citalopram has an Antagonistic Action on Cortical Spreading Depression in Well-nourished and Early-malnourished Adult Rats

2002 ◽  
Vol 5 (2) ◽  
pp. 115-123 ◽  
Author(s):  
R.C.A. Guedes ◽  
A. Amâncio-Dos-Santos ◽  
R. Manhães-De-Castro ◽  
R.R.G. Costa-Cruz
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Adult Rats ◽  
Antagonistic Action

Hypercaloric high-lipid diet and brain development: Effects on cortical spreading depression in adult rats

2013 ◽  
Vol 16 (6) ◽  
pp. 275-281 ◽  
Author(s):  
Paula Catirina Pereira da Silva Germano ◽  
Débora de Lima e Silva ◽  
Geórgia de Sousa Ferreira Soares ◽  
Ângela Amâncio dos Santos ◽  
Rubem Carlos Araújo Guedes
Keyword(s):  
Brain Development ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Adult Rats ◽  
High Lipid ◽  
High Lipid Diet ◽  
Lipid Diet

scholarly journals Cerebral Blood Flow Changes during Cortical Spreading Depression are Not Altered by Inhibition of Nitric Oxide Synthesis

1994 ◽  
Vol 14 (6) ◽  
pp. 939-943 ◽  
Author(s):  
Zheng Gang Zhang ◽  
Michael Chopp ◽  
Kenneth I. Maynard ◽  
Michael A. Moskowitz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Arterial Blood ◽  
Nos Inhibitors ◽  
Before And After ◽  
Male Wistar Rats

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-l-arginine (L-NNA) or N-nitro-l-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.

scholarly journals Dynamic diameter response of intraparenchymal penetrating arteries during cortical spreading depression and elimination of vasoreactivity to hypercapnia in anesthetized mice

2016 ◽  
Vol 37 (2) ◽  
pp. 657-670 ◽  
Author(s):  
Miyuki Unekawa ◽  
Yutaka Tomita ◽  
Kazuto Masamoto ◽  
Haruki Toriumi ◽  
Takashi Osada ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cortical Spreading Depression ◽  
Regional Cerebral Blood Flow ◽  
Spreading Depression ◽  
Regional Cerebral Blood ◽  
Basal Diameter ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Dynamic Diameter ◽  
Current Potential

Cortical spreading depression (CSD) induces marked hyperemia with a transient decrease of regional cerebral blood flow (rCBF), followed by sustained oligemia. To further understand the microcirculatory mechanisms associated with CSD, we examined the temporal changes of diameter of intraparenchymal penetrating arteries during CSD. In urethane-anesthetized mice, the diameter of single penetrating arteries at three depths was measured using two-photon microscopy during passage of repeated CSD, with continuous recordings of direct current potential and rCBF. The first CSD elicited marked constriction superimposed on the upstrokes of profound dilation throughout each depth of the penetrating artery, and the vasoreaction temporally corresponded to the change of rCBF. Second or later CSD elicited marked dilation with little or no constriction phase throughout each depth, and the vasodilation also temporally corresponded to the increase of rCBF. Furthermore, the peak dilation showed good negative correlations with basal diameter and increase of rCBF. Vasodilation induced by 5% CO2 inhalation was significantly suppressed after CSD passage at any depth as well as hyperperfusion. These results may indicate that CSD-induced rCBF changes mainly reflect the diametric changes of the intraparenchymal arteries, despite the elimination of responsiveness to hypercapnia.

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