Repetitive Spreading Depression Research Articles

Histopathological Findings of Sodium Valproate and Dexamethasone on Repetitive Spreading Depression Induced by POTASSIUM HYDROCHLORIDE in Juvenile RATS

Histopathological Findings of Sodium Valproate and Dexamethasone on Repetitive Spreading Depression Induced by POTASSIUM HYDROCHLORIDE in Juvenile RATS

REMOVED: Behavioral effect of DNQX, AMPA receptor antagonist, on repetitive spreading depression in juvenile rats

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Spreading Depression Mimics the Behavioral Features of Schizophrenia

Spreading depression (SD) known as an evoked neuronal activity and changes in ionic, metabolic and hemodynamic characteristics of the brain. From a clinical perspective SD plays a pathophysiological role in several neurological disorders, e.g., migraine, epilepsy, and spinal cord disease. Pronounced release of dopamine in mesolimbic pathway, remarkably in nucleus accumbens during SD and the noted role of increased dopamine in schizophrenia suggests that SD could be a predisposing factor for the occurrence of schizophrenia. To test this hypothesis, male Wistar rats (60-80gr) randomly chosen in 3 groups. For induction of repetitive SD, 3 mol/L KCl was injected four times in rats during 4 weeks. After 4 weeks rats’ anxiety were evaluated using elevated plus-maze. Furthermore, all three groups of rats spent comparable times in social contact in order to determine social interaction. In the present study, we also tested the possible effect of SD induction on prepulse inhibition (PPI). SD induced rats had decreased threshold of anxiety in comparison with control group. The percentage of aggressive behavior was also increased in SD induced rats. Finally, the amount of prepulse inhibition was decreased significantly in SD group of animals. The results suggest that SD can mimic some behavioral features of schizophrenia and might be a useful animal model in the study of this disease. We conclude that Spreading depression potentiates to be a kind of useful way for making a new model of schizophrenia and this can used in different basic and clinical researches in the field of schizophrenia.

EHMTI-0094. Effect of nifedipine on memory impairment induced by repetitive spreading depression

Spreading depression (SD) is known by transient loss of spontaneous and evoked neuronal activity and changes in ionic, metabolic and hemodynamic characteristics of the brain. It has been shown that repetitive SD produced memory deficits in juvenile rats. Furthermore, the role of Ca2+channels on induction and propagation of SD was investigated by several scientists. The aim of the present study was to study the role of a Ca2+channel-blocker, nifedipine, on memory deficits induced by repetitive SD.

Effect of Sumatriptan on Learning and Memory Impairment Resulting from Repetitive Spreading Depression

Effect of Sumatriptan on Learning and Memory Impairment Resulting from Repetitive Spreading Depression

Effect of Nifedipine on Memory Impairment Induced by Repetitive Spreading Depression

Effect of Nifedipine on Memory Impairment Induced by Repetitive Spreading Depression

Assessment of AMPA Receptor Antagonist Administration on Spatial Memory of Juvenile Rats Induced Repetitive Spreading Depression

Assessment of AMPA Receptor Antagonist Administration on Spatial Memory of Juvenile Rats Induced Repetitive Spreading Depression

The Effect of MK-801 on Memory after Induction of Repetitive Spreading Depression in the Juvenile Rat

The Effect of MK-801 on Memory after Induction of Repetitive Spreading Depression in the Juvenile Rat

Ca2 + channel-blockers counter with the damaging effect of repetitive spreading depression on memory

Background and purpose: Spreading depression known by transient loss of spontaneous and evoked neuronal activity and changes in ionic, metabolic and hemodynamic characteristics of the brain. Many studies have focused on the role of Ca2+ channels in spreading depression, however this role is not completely clear yet. On the other hand it has proven that impairment of memory is one of the main effects of spreading depression. In our study we aimed at determining the role of Ca2+ channel-blockers on repetitive spreading depression in terms of its effect on memory.

Dexamethasone multifunctional role in spreading depression

Spreading depression (SD) is a neural hyperexc/INS;itabi/INS;lity, which spreads/INS; to adjoining area of brain cortical; slowly continues/INS; through the brain and changes /INS;neural electrical and metabolic activity. It has been proved that SD plays/INS; a dramatic role in some neurological disorder through the changes it causes/INS;. Previous studies applied various types of drugs through diverse pharmacological aspects to relieve /INS;SD wave distribution. However most have been abort due to their unpleasant side effects. In the present study we seek for dexamethasone's (Dex) multifunctional properties in order to protect cellular damage and/INS; then prevent even other neurological disorder accuracy following SD. Animals/INS; were /INS;randomly divided into five groups/INS; including /INS;CTRLs, sham, spreading depression and dexamethasone treatment group. Animals/INS; were anesthetized and a /INS;cannula as well as an /INS;electrode was /INS;established above the brain cortex. Intracerebral KCl was used to induce repetitive cortical SD for 4 continuous week. Following each induction memory retrieval tests/INS; (T-maze) were done. The brains were removed after 4 weeks. Histopathologically estimation was used to testify dexamethasone effect. In addition dexamethasone effects on blood brain barer (BBB) to facilitate /INS;substance recovery in cerebral fluid were tested by Evans blue. By repetitive SD memory retrieval was impaired due to increscent of dark neural seen in several regions of juvenile rat brain. Besides/INS; that brain electrical activity determination showed slake of neural activity after SD induction. Neural cell recoveries after SD due to increscent of substance passage through BBB were promoted/INS;.

Role of Dexamethasone on Repetitive Spreading Depression in Juvenile Wistar Rat

Role of Dexamethasone on Repetitive Spreading Depression in Juvenile Wistar Rat

Neuronal death by repetitive cortical spreading depression in juvenile rat brain

Spreading depression (SD) is an intrinsic bioelectrical property of the human central nervous system, which plays a key role in neurological disorders. In the present study, we investigated whether experimentally induced repetitive SD caused neuronal death in cortical and subcortical regions of the juvenile rat brain. The animals were anesthetized and the electrodes as well as a cannula were implanted over the brain. Repetitive cortical SD events were induced by KCl injection. The brains were removed after 4weeks. Repetitive SD enhanced the production of dark neurons, reduced the mean volume of normal neurons, increased the number of apoptotic neurons, and enhanced expression of the NR2B subunit of NMDA receptors as well as the GluR1 subunit of AMPA receptors in various regions of the juvenile rat brain. In addition, induction of repetitive SD enhanced long-term potentiation in CA1 hippocampal area. We observed a correlation between cell injury/neuronal death induced by repetitive SD and changes in glutamate receptor expression. The data indicate that repetitive cortical SD in juvenile rats causes neuronal damage in both cortical and subcortical areas of the brain. This may play an important role in the pathophysiology of SD-related neurological disorders, especially in children.

Spreading depression and related events are significant sources of neuronal Zn2+ release and accumulation.

Spreading depression (SD) involves coordinated depolarizations of neurons and glia that propagate through the brain tissue. Repetitive SD-like events are common following human ischemic strokes, and are believed to contribute to the enlargement of infarct volume. Accumulation of Zn(2+) is also implicated in ischemic neuronal injury. Synaptic glutamate release contributes to SD propagation, and because Zn(2+) is costored with glutamate in some synaptic vesicles, we examined whether Zn(2+) is released by SD and may therefore provide a significant source of Zn(2+) in the postischemic period. Spreading depression-like events were generated in acutely prepared murine hippocampal slices by deprivation of oxygen and glucose (OGD), and Zn(2+) release was detected extracellularly by a Zn(2+)-selective indicator FluoZin-3. Deprivation of oxygen and glucose-SD produced large FluoZin-3 increases that propagated with the event, and signals were abolished in tissues from ZnT3 knockout animals lacking synaptic Zn(2+). Synaptic Zn(2+) release was also maintained with repetitive SDs generated by microinjections of KCl under normoxic conditions. Intracellular Zn(2+) accumulation in CA1 neurons, assessed using microinjection of FluoZin-3, showed significant increases following SD that was attributed to synaptic Zn(2+) release. These results suggest that Zn(2+) is released during SDs and could provide a significant source of Zn(2+) that contributes to neurodegeneration in the postischemic period.

The effect of repetitive spreading depression on neuronal damage in juvenile rat brain

Spreading depression (SD) is pronounced depolarization of neurons and glia that travels slowly across brain tissue followed by massive redistribution of ions between intra- and extracellular compartments. There is a relationship between SD and some neurological disorders. In the present study the effects of repetitive SD on neuronal damage in cortical and subcortical regions of juvenile rat brain were investigated. The animals were anesthetized and the electrodes as well as cannula were implanted over the brain. SD-like event was induced by KCl injection. The brains were removed after 2 or 4 weeks after induction of 2 or 4 SD-like waves (with interval of 1 week), respectively. Normal saline was injected instead of KCl in sham group. For stereological study, paraffin-embedded brains were cut in 5 μm sections. The sections were stained with Toluidine Blue to measure the volume-weighted mean volume of normal neurons and the numerical density of dark neurons. The volume-weighted mean volume of normal neurons in the granular layer of the dentate gyrus and layer V of the temporal cortex in SD group were significantly decreased after four repetitive SD. Furthermore, densities of dark neurons in the granular layer of the dentate gyrus (after 2 weeks), the caudate–putamen, and layer V of the temporal cortex (after 4 weeks) were significantly increased in SD group. Repetitive cortical SD in juvenile rats may cause neuronal damage in cortical and subcortical areas of the brain. This may important in pathophysiology of SD-related neurological disorders.

Microarray‐based long‐term detection of genes differentially expressed after cortical spreading depression

Spreading depression (SD) is a slowly propagating wave of neuronal depolarization altering ion homeostasis, blood flow and energy metabolism without causing irreversible damage of the tissue. As SD has been implicated in several neurological diseases including migraine and stroke, understanding these disorders requires systematic knowledge of the processes modified by SD. Thus, we induced repetitive SD in the rat cerebral cortex by topical application of 3 m KCl for approximately 2 h and evaluated the kinetics of SD-induced changes in cortical gene expression for up to 30 days using Affymetrix RAE230A arrays. The temporal profile showed a rapid expression of immediate early genes, genes associated with inflammation, metabolism, stress and DNA repair, ion transport, and genes that play a role in growth/differentiation. Stress-response genes could still be detected after 24 h. At this time, induced genes were mainly related to the cell membrane and adhesion, or to the cytoskeleton. A subset of genes was still affected even 30 days after SD. Real-time polymerase chain reactions and immunohistochemistry confirmed the microarray results for several of the transcripts. Our findings demonstrate a temporal pattern of gene expression which might promote tissue remodeling and cortical plasticity, and might probably account for the mediation of neuronal tolerance towards subsequent ischemia.

Is Spreading Depression Bad for You?Focus on “Repetitive Normoxic Spreading Depression-Like Events Result in Cell Damage in Juvenile Hippocampal Slice Cultures”

In this issue of the Journal of Neurophysiology (p. x), Pomper et al. report that repeated episodes of spreading depression-like events (SDLEs) caused irreversible injury in hippocampal slice cultures taken from immature brains. Although after the first four or five SDLEs, antidromic population

Recurrent spreading depression (SD) causes early opening of the blood-brain barrier (BBB)

SD is a depolarization wave propagating at a rate of about 3 mm/min in the cerebral cortex. It is characterized by an amplitude reduction of the electrocorticographic activity, a rise of the extracellular potassium to 60 mM and a reduction of the extracellular volume. Typical changes of cerebral blood flow (CBF) accompany SD, which consist of a short lasting spreading hyperemia followed by a long lasting spreading oligemia. SD is triggered by electrical, mechanical or toxic factors and is probably involved in the pathogenesis of migraine, focal ischemia, head trauma and cerebral hemorrhage. SD is assumed to be the pathophysiological correlate of the migraine aura. We have recently observed a patient with familial hemiplegic migraine (FHM) type II and a long-lasting migraine aura with fluctuating neurological symptoms. Quantitative analysis of early gadolinium-enhanced MR images revealed a left-hemispheric, cortical blood brain-barrier (BBB) disruption preceding delayed cortical edema in this ATP1A2 mutation carrier. As we know from the work by Strong et al. repetitive SDs can occur in the human brain tissue, which could explain the fluctuating symptoms in our FHM patient. Additionally, a recent publication by Gursoy-Ozdemir et al. showed a delayed enhancement of BBB permeability and subsequent cortical oedema following a single SD. Based on these observations, we studied here whether recurrent SD causes early BBB disruption in the rat cortex in vivo. We triggered SD with artificial cerebrospinal fluid (ACSF) containing a potassium concentration ([K+]ACSF) of 130 mM at an open parietal cranial window. SDs were monitored with an intracortical potassium sensitive microelectrode and laser-Doppler flowmetry. We also recorded the propagation of SDs to a distant closed frontal cranial window using an epidural Ag-AgCl electrode. BBB integrity was evaluated quantitatively by analyzing fluorescence in brain sections following the peripheral injection of Evan's Blue or Lucifer yellow. At the occipital window, [K+]ACSF evoked several SDs in all animals. In the first group (n = 10), one or more SDs propagated to the frontal window. In contrast, in the second group (n = 9), pretreatment with MK-801 (5 mg/kg BW i.v.), abolished SD propagation. Within two hours after the onset of the first SD, significantly enhanced fluorescence intensity at the frontal cortex was only measured in animals from group 1 with multiple propagated SDs. In conclusion, we provide evidence that repetitive SDs significantly increase blood-brain barrier permeability within two hours after the onset.

Spreading depression activates unfolded protein response

Preconditioning is a process where a preceding non-lethal form of stress activates a stress response that protects cells against an otherwise lethal form of stress. Preconditioning can be induced in various ways including short-term ischemia or spreading depression. Here we investigated the effect of 1h repetitive spreading depression on the unfolded protein response (UPR), a stress response activated under conditions associated with endoplasmic reticulum (ER) dysfunction. Spreading depression induced processing of xbp1 mRNA, indicative of an activation of UPR. Processing of xbp1 was paralleled by a rise in grp78 mRNA levels resulting from an activation of a signal transduction pathway that depends on protein synthesis. Preconditioning-induced activation of UPR may preserve ER functioning under pathological conditions interfering with ER functions.

Changes in Nestin and AMPA receptors are associated with preconditioning of the mouse cortex by repetitive spreading depression

Conference Abstract| June 01 2002 Changes in Nestin and AMPA receptors are associated with preconditioning of the mouse cortex by repetitive spreading depression P. L. Chazot; P. L. Chazot 1Institute of Pharmacy, University of Sunderland, Sunderland, SR2 3SD; School of Pharmacy, University of Bradford, Bradford, BD7 1DP Search for other works by this author on: This Site PubMed Google Scholar O. V. Godukhin; O. V. Godukhin 1Institute of Pharmacy, University of Sunderland, Sunderland, SR2 3SD; School of Pharmacy, University of Bradford, Bradford, BD7 1DP Search for other works by this author on: This Site PubMed Google Scholar T. P. Obrenovitch T. P. Obrenovitch 1Institute of Pharmacy, University of Sunderland, Sunderland, SR2 3SD; School of Pharmacy, University of Bradford, Bradford, BD7 1DP Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (2002) 30 (3): A70. https://doi.org/10.1042/bst030a070c Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation P. L. Chazot, O. V. Godukhin, T. P. Obrenovitch; Changes in Nestin and AMPA receptors are associated with preconditioning of the mouse cortex by repetitive spreading depression. Biochem Soc Trans 1 June 2002; 30 (3): A70. doi: https://doi.org/10.1042/bst030a070c Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 2002 Biochemical Society2002 Article PDF first page preview Close Modal You do not currently have access to this content.

Changes in Nestin and AMPA receptors are associated with preconditioning of the mouse cortex by repetitive spreading depression

Changes in Nestin and AMPA receptors are associated with preconditioning of the mouse cortex by repetitive spreading depression