Spreading depression in vivo potentiates electrically-driven responses in frog optic tectum

2005 ◽  
Vol 1036 (1-2) ◽  
pp. 109-114 ◽  
Author(s):  
Rubem Carlos Araújo Guedes ◽  
Kazuya Tsurudome ◽  
Nobuyoshi Matsumoto
Keyword(s):  
Optic Tectum ◽  
Spreading Depression

In Vivo Monitoring of Oxygen Fluctuation Simultaneously at Multiple Sites of Rat Cortex during Spreading Depression

2018 ◽  
Vol 90 (22) ◽  
pp. 13783-13789 ◽  
Author(s):  
Tongfang Xiao ◽  
Xianchan Li ◽  
Huan Wei ◽  
Wenliang Ji ◽  
Qingwei Yue ◽  
...  
Keyword(s):  
Spreading Depression ◽  
Rat Cortex ◽  
In Vivo Monitoring

scholarly journals In Vivo Uptake of [3H]Nimodipine into Brain during Cortical Spreading Depression

1997 ◽  
Vol 17 (5) ◽  
pp. 586-590 ◽  
Author(s):  
Sachiko Osuga ◽  
Antoine M. Hakim ◽  
Hitoshi Osuga ◽  
Matthew J. Hogan
Keyword(s):  
Rat Brain ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Control Group ◽  
Similar Measurement ◽  
Contralateral Hemisphere ◽  
Radiotracer Uptake ◽  
Uptake Studies ◽  
In Vivo Uptake

We report autoradiographic measurements of the in vivo uptake of [3H]nimodipine during the nonischemic depolarization of cortical spreading depression (CSD) in rat brain. [3H]Nimodipine uptake in brain was determined regionally in rats undergoing CSD (n = 8) and was significantly increased in cortex (14 ± 7%) and hippocampus (10 ± 6%) on the stimulated side relative to the contralateral hemisphere when compared with the same measurements in a control group (n = 8). A similar measurement using the physiologically inert radiotracer [14C]iodoantipyrine to control for potential effects of CSD on radioligand distribution showed a minimal increase (2.4 ± 0.7%) of radiotracer uptake in cortex after CSD. This increase was significantly less than that observed in the [3H]nimodipine uptake studies. We hypothesize that increased in vivo [3H]nimodipine uptake in CSD identifies regions of depolarization and thus infers activation of the L-type voltage sensitive calcium channels.

Diffusion-Weighted MRI Used to Detect in Vivo Modulation of Cortical Spreading Depression: Comparison of Sumatriptan and Tonabersat

2001 ◽  
Vol 172 (2) ◽  
pp. 342-353 ◽  
Author(s):  
Daniel P. Bradley ◽  
Martin I. Smith ◽  
Chaiyapoj Netsiri ◽  
Justin M. Smith ◽  
Kurt H.J. Bockhorst ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Diffusion Weighted Mri ◽  
Diffusion Weighted

Biochemical Effects of Cerebral Ischemia: Relevance To Migraine

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 35-42 ◽  
Author(s):  
KMA Welch ◽  
JA Helpern ◽  
JR Ewing ◽  
WM Robertson ◽  
G D'Andrea
Keyword(s):  
Energy Metabolism ◽  
Cerebral Ischemia ◽  
Spreading Depression ◽  
Metabolic Depression ◽  
Ischemia And Reperfusion ◽  
Phosphate Metabolism ◽  
Biochemical Effects ◽  
The Brain ◽  
Intracranial Circulation

Although decreased CBF has now been reported during the prodrome of migraine, the cause of the decreased flow is still unknown. It is particularly unclear whether these phenomena are related to vasospasm and “steal” between the extracranial and intracranial circulation or to the spreading depression of Leao and the accompanying metabolic depression. In the present paper, metabolic changes in the brain during ischemia and reperfusion are reviewed and compared with CNS biochemical changes during migraine attack. In addition, the technique of Topical Magnetic Resonance (TMR) as applied to the in vivo study of energy phosphate metabolism in extracranial tissues and brain is described and the potential of this technique to evaluate shifts in energy metabolism and pH in stroke and migraine is discussed.

Light-Induced Calcium Influx Into Retinal Axons Is Regulated by Presynaptic Nicotinic Acetylcholine Receptor Activity In Vivo

1999 ◽  
Vol 81 (2) ◽  
pp. 895-907 ◽  
Author(s):  
James A. Edwards ◽  
Hollis T. Cline
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Visual Stimulus ◽  
Optic Tectum ◽  
Visual Stimulation ◽  
Calcium Influx ◽  
Nicotinic Acetylcholine ◽  
Retinal Axons ◽  
Retinotectal System

Light-induced calcium influx into retinal axons is regulated by presynaptic nicotinic acetylcholine receptor activity in vivo. Visual activity is thought to be a critical factor in controlling the development of central retinal projections. Neuronal activity increases cytosolic calcium, which was hypothesized to regulate process outgrowth in neurons. We performed an in vivo imaging study in the retinotectal system of albino Xenopus laevis tadpoles with the fluorescent calcium indicator calcium green 1 dextran (CaGD) to test the role of calcium in regulating axon arbor development. We find that visual stimulus to the retina increased CaGD fluorescence intensity in retinal ganglion cell (RGC) axon arbors within the optic tectum and that branch additions to retinotectal axon arbors correlated with a local rise in calcium in the parent branch. We find three types of responses to visual stimulus, which roughly correlate with theon, off, and sustained response types of RGC reported by physiological criteria. Imaging in bandscan mode indicated that patterns of calcium transients were nonuniform throughout the axons. We tested whether the increase in calcium in the retinotectal axons required synaptic activity in the retina; intraocular application of tetrodotoxin (10 μM) or nifedipine (1 and 10 μM) blocked the stimulus-induced increase in RGC axonal fluorescence. A second series of pharmacological investigations was designed to determine the mechanism of the calcium elevation in the axon terminals within the optic tectum. Injection of bis-( o-aminophenoxy)- N, N, N′, N′-tetraacetic acid-AM (BAPTA-AM) (20 mM) into the tectal ventricle reduced axonal calcium levels, supporting the idea that visual stimulation increases axonal calcium. Injection of BAPTA (20 mM) into the tectal ventricle to chelate extracellular calcium also attenuated the calcium response to visual stimulation, indicating that calcium enters the axon from the extracellular medium. Caffeine (10 mM) caused a large increase in axonal calcium, indicating that intracellular stores contribute to the calcium signal. Presynaptic nicotinic acetylcholine receptors (nAChRs) may play a role in axon arbor development and the formation of the topographic retinotectal projection. Injection of nicotine (10 μM) into the tectal ventricle significantly elevated RGC axonal calcium levels, whereas application of the nAChR antagonist αBTX (100 nM) reduced the stimulus-evoked rise in RGC calcium fluorescence. These data suggest that light stimulus to the retina increases calcium in the axon terminal arbors through a mechanism that includes influx through nAChRs and amplification by calcium-induced calcium release from intracellular calcium stores. Such a mechanism may contribute to developmental plasticity of the retinotectal system by influencing both axon arbor elaboration and the strength of synaptic transmission.

scholarly journals Targeting the Zebrafish Optic Tectum Using In Vivo Electroporation

2010 ◽  
Vol 2010 (7) ◽  
pp. pdb.prot5463-pdb.prot5463 ◽  
Author(s):  
K. J. Hoegler ◽  
J. H. Horne
Keyword(s):  
Optic Tectum ◽  
In Vivo Electroporation ◽  
Zebrafish Optic Tectum

scholarly journals High Speed Diffusion Magnetic Resonance Imaging of Ischemia and Spontaneous Periinfarct Spreading Depression after Thromboembolic Stroke in the Rat

2000 ◽  
Vol 20 (12) ◽  
pp. 1636-1647 ◽  
Author(s):  
Andreas Kastrup ◽  
Tobias Neumann-Haefelin ◽  
Michael E. Moseley ◽  
Alex de Crespigny
Keyword(s):  
Temporal Resolution ◽  
High Speed ◽  
Spreading Depression ◽  
Tissue Injury ◽  
Lesion Volume ◽  
Thromboembolic Stroke ◽  
Ischemic Lesion ◽  
Intracellular Space ◽  
Ischemic Core

Spontaneous episodes of transient cell membrane depolarization (spreading depression [SD]) occur in the surroundings of experimental stroke lesions and are believed to contribute to infarct growth. Diffusion-weighted imaging (DWI) is capable of detecting the water shifts from extracellular to intracellular space associated with SD waves and ischemia, and can make in vivo measurements of these two features on a pixel-by-pixel basis with good temporal resolution. Using continuous high speed DWI with a temporal resolution of 12 seconds over a period of 3 hours, the in vivo contribution of spontaneous SDs to the development of ischemic tissue injury was examined in 8 rats using a thromboembolic stroke model. During the observation period, the initial lesion volume increased in 4 animals, remained unchanged in 1 animal, and decreased in 3 animals (most likely because of spontaneous clot lysis). Irrespective of the lesion evolution patterns, animals demonstrated 6.5 ± 2.1 spontaneous SDs outside of the ischemic core. A time-to-peak analysis of apparent diffusion coefficient (ADC) changes for each SD wave demonstrated multidirectional propagation patterns from variable initiation sites. Maps of the time constants of ADC recovery, reflecting the local energy supply and cerebral blood flow, revealed prolonged recovery times in areas close to the ischemic core. However, repetitive SD episodes in the periinfarct tissue did not eventually lead to permanent ADC reductions. These results suggest that spontaneous SD waves do not necessarily contribute to the expansion of the ischemic lesion volume in this model.

Potentiation of spontaneous and evoked cortical electrical activity after spreading depression: in vivo analysis in well-nourished and malnourished rats

2011 ◽  
Vol 214 (3) ◽  
pp. 463-469 ◽  
Author(s):  
Thays Kallyne Marinho de Souza ◽  
Mariana Barros e Silva ◽  
André Ricardson Gomes ◽  
Hélio Magalhães de Oliveira ◽  
Renato Barros Moraes ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Spreading Depression ◽  
Cortical Electrical Activity ◽  
In Vivo Analysis

scholarly journals Hypoxia Tolerance Declines with Age in the Absence of Methionine Sulfoxide Reductase (MSR) in Drosophila melanogaster

2021 ◽  
Author(s):  
Nirthieca Suthakaran ◽  
Sanjana Chandran ◽  
Michael Iacobelli ◽  
David Binninger
Keyword(s):  
Drosophila Melanogaster ◽  
Recovery Time ◽  
Spreading Depression ◽  
Tissue Injury ◽  
Methionine Sulfoxide ◽  
Methionine Sulfoxide Reductase ◽  
Hypoxia Tolerance ◽  
Mammalian Brain ◽  
Apoptotic Pathway

Unlike the mammalian brain, Drosophila melanogaster can tolerate several hours of hypoxia without any tissue injury by entering a protective coma known as spreading depression. However, when oxygen is reintroduced, there is an increased production of reactive oxygen species (ROS) that causes oxidative damage. Methionine sulfoxide reductase (MSR) acts to restore functionality to oxidized methionine residues. In the present study, we have characterized in vivo effects of MSR deficiency on hypoxia tolerance throughout the lifespan of Drosophila. Flies subjected to sudden hypoxia that lacked MSR activity exhibited a longer recovery time and a reduced ability to survive hypoxic stress as they approached senescence. However, when hypoxia was induced slowly, MSR deficient flies recovered significantly quicker throughout their entire adult lifespan. In addition, the wildtype and MSR deficient flies had nearly 100% survival rates throughout their lifespan. Neuroprotective signaling mediated by decreased apoptotic pathway activation, as well as gene reprogramming and metabolic downregulation are possible reasons for why MSR deficient flies have faster recovery time and a higher survival rate upon slow induction of spreading depression. Our data are the first to suggest important roles of MSR and longevity pathways in hypoxia tolerance exhibited by Drosophila.

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