scholarly journals Evidence that adenosine contributes to Leao’s spreading depression in vivo

2016 ◽  
Vol 37 (5) ◽  
pp. 1656-1669 ◽  
Author(s):  
Britta E Lindquist ◽  
C William Shuttleworth
Keyword(s):  
Action Potential ◽  
Adenosine Deaminase ◽  
Neuronal Activity ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Secondary Phase ◽  
Competitive Antagonist ◽  
Postsynaptic Potentials ◽  
Evoked Activity

Leao’s spreading depression of cortical activity is a propagating silencing of neuronal activity resulting from spreading depolarization (SD). We evaluated the contributions of action potential (AP) failure and adenosine A1 receptor (A1R) activation to the depression of evoked and spontaneous electrocorticographic (ECoG) activity after SD in vivo, in anesthetized mice. We compared depression with SD-induced effects on AP-dependent transmission, and synaptic potentials in the transcallosal and thalamocortical pathways. After SD, APs recovered rapidly, within 1–2 min, as demonstrated by evoked activity in distant projection targets. Evoked corticocortical postsynaptic potentials recovered next, within ∼5 min. Spontaneous ECoG and evoked thalamocortical postsynaptic potentials recovered together, after ∼10–15 min. The duration of ECoG depression was shortened 20% by systemic (10 mg/kg) or focal (30 µM) administration of A1R competitive antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). ECoG depression was also shortened by focal application of exogenous adenosine deaminase (ADA; 100 U/mL), and conversely, was prolonged 50% by the non-competitive ADA inhibitor deoxycoformycin (DCF; 100 µM). We concluded that while initial depolarization block is brief, adenosine A1R activation, in part, contributes to the persistent secondary phase of Leao’s cortical spreading depression.

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

Physiological properties of rat ventral pallidal neurons recorded intracellularly in vivo

1996 ◽  
Vol 75 (4) ◽  
pp. 1432-1443 ◽  
Author(s):  
A. Lavin ◽  
A. A. Grace
Keyword(s):  
B Cells ◽  
Nucleus Accumbens ◽  
Action Potential ◽  
Type A ◽  
C Cells ◽  
Postsynaptic Potentials ◽  
A Cells ◽  
Type C ◽  
Stimulation Of

1. The physiology of ventral pallidal (VP) cells was investigated using in vivo intracellular recording and staining techniques in adult rats. Based on electrophysiological criteria, three different types of cells were found: type A cells, which fired phasic spikes that did not exhibit a substantial afterhyperpolarization (AHP), type B cells, which exhibited a slow ramplike depolarization that preceded the short-duration action potential; the spike was followed by a prominent AHP, and type C cells, which were the only cells that fired spikes in couplets or bursts, with the spikes in a burst exhibiting a progressive increase in duration and a decrease in amplitude. These cells also exhibited a rebound low threshold spikelike event. Furthermore, 18% of the VP cells recorded exhibited a slow subthreshold oscillation of the membrane potential (< 1 Hz). 2. The response of VP cells to stimulation of fibers arising from the prefrontal cortex, nucleus accumbens, and mediodorsal thalamic nucleus (MD) was examined. In contrast to our initial predictions, all cells responded to nucleus accumbens stimulation with excitation. Type A and B cells responded to nucleus accumbens stimulation with excitation and to MD stimulation with antidromic-like responses, orthodromic excitation, or evoked inhibitory postsynaptic potentials. Only type A cells responded to prefrontal cortical stimulation. Type C cells only responded to stimulation of the nucleus accumbens, which resulted in evoked excitatory postsynaptic potentials. 3. The cells in the VP therefore can be segregated into three physiologically defined groups according to action potential discharge patterns and their response to afferent fiber stimulation.

scholarly journals A dual role for α-synuclein in facilitation and depression of dopamine release from substantia nigra neurons in vivo

2020 ◽  
Vol 117 (51) ◽  
pp. 32701-32710
Author(s):  
Mahalakshmi Somayaji ◽  
Stefano Cataldi ◽  
Se Joon Choi ◽  
Robert H. Edwards ◽  
Eugene V. Mosharov ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Action Potential ◽  
Synaptic Vesicle ◽  
Neuronal Activity ◽  
Dopamine Release ◽  
Short Intervals ◽  
Presynaptic Plasticity ◽  
Presynaptic Calcium ◽  
Synaptic Vesicle Fusion

α-Synuclein is expressed at high levels at presynaptic terminals, but defining its role in the regulation of neurotransmission under physiologically relevant conditions has proven elusive. We report that, in vivo, α-synuclein is responsible for the facilitation of dopamine release triggered by action potential bursts separated by short intervals (seconds) and a depression of release with longer intervals between bursts (minutes). These forms of presynaptic plasticity appear to be independent of the presence of β- and γ-synucleins or effects on presynaptic calcium and are consistent with a role for synucleins in the enhancement of synaptic vesicle fusion and turnover. These results indicate that the presynaptic effects of α-synuclein depend on specific patterns of neuronal activity.

scholarly journals Increased calcium influx triggers and accelerates cortical spreading depression in vivo in male adult rats

2014 ◽  
Vol 558 ◽  
pp. 87-90 ◽  
Author(s):  
Daniel Torrente ◽  
Rosângela Figueiredo Mendes-da-Silva ◽  
Andréia Albuquerque Cunha Lopes ◽  
Janneth González ◽  
George E. Barreto ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Calcium Influx ◽  
Adult Rats ◽  
Male Adult

scholarly journals Cortical Spreading Depression Can Be Triggered by Sensory Stimulation in Primed Wild Type Mouse Brain: a Mechanistic Insight to Migraine Aura Generation

2021 ◽  
Author(s):  
Sahin Hanalioglu ◽  
Aslihan Taskiran-Sag ◽  
Hulya Karatas ◽  
Buket Donmez-Demir ◽  
Sinem Yilmaz-Ozcan ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Glutamate Release ◽  
Wild Type Mouse ◽  
Sensory Stimulation ◽  
Photic Stimulation ◽  
Normal Brain ◽  
Whisker Stimulation

Abstract Background: Unlike the spontaneously appearing aura in migraineurs, experimentally, cortical spreading depression (CSD), the neurophysiological correlate of aura is induced by non-physiological stimuli. Consequently, neural mechanisms involved in spontaneous CSD generation, which may provide insight how migraine starts in an otherwise healthy brain, remains largely unclear. We hypothesized that CSD can be physiologically induced by sensory stimulation in primed mouse brain. Methods: Cortex was made susceptible to CSD with partial inhibition of Na+/K+-ATPase by epidural application of a low dose of Na+/K+-ATPase blocker ouabain that does not induce repetitive CSDs or by knocking-down α2 subunit of Na+/K+-ATPase, which is crucial for K+ and glutamate re-uptake by astrocytes, with shRNA. Stimulation-induced CSDs and extracellular K+ changes were monitored in vivo electrophysiologically or with a K+-sensitive fluoroprobe (IPG-4). Results: After priming with ouabain, photic stimulation increased the CSD incidence compared with non-stimulated animals (44.0 vs. 4.9%, p<0.001). Whisker stimulation was less effective (14.9 vs. 2.4%, p=0.02). Knocking-down Na+/K+-ATPase (50% decrease in mRNA) lowered the CSD threshold in all mice tested but triggered stimulus-induced CSDs in 14.3% and 16.7% of mice with photic and whisker stimulation, respectively. Confirming Na+/K+-ATPase hypofunction, extracellular K+ significantly rose during stimulation after subthreshold ouabain or shRNA treatment unlike controls. In line with higher CSD susceptibility, K+ rise was more prominent after ouabain. To gain insight to preventive mechanisms reducing the incidence of stimulus-induced CSDs, we applied an A1-receptor (DPCPX) or GABA-A (bicuculine) antagonist over the occipital cortex, because adenosine formed during stimulation or inhibitory interneuron activity can reduce CSD susceptibility. DPCPX induced CSDs or CSD-like small-DC shifts during photic stimulation, whereas bicuculine was not effective. Conclusions: Our findings indicate that normal brain is well protected against CSD generation. For CSD to be ignited under physiological conditions, priming and predisposing factors are required as seen in migraine patients. Intense sensory stimulation has the potential to trigger a CSD when co-existing conditions can bring extracellular K+ and glutamate concentrations over threshold via reduced uptake of K+ and glutamate (e.g. inefficient fueling of α2-Na+/K+-ATPase due to reduced glycogen breakdown) or facilitated glutamate release (e.g. reduced presynaptic adenosinergic inhibition).

scholarly journals Chlorella vulgaris functional alcoholic beverage: Effect on propagation of cortical spreading depression and functional properties

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255996
Author(s):  
Danielli M. M. Dantas ◽  
Thiago B. Cahú ◽  
Carlos Yure B. Oliveira ◽  
Ricardo Abadie-Guedes ◽  
Nathalia A. Roberto ◽  
...  
Keyword(s):  
Chlorella Vulgaris ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Alcoholic Beverage ◽  
Food Additives ◽  
Radical Scavenging ◽  
Protective Role ◽  
Bioactive Molecules

Recent advances in microalgae biotechnology have proven that these microorganisms contain a number of bioactive molecules, that can be used as food additives that help prevent disease. The green microalga Chlorella vulgaris presents several biomolecules, such as lutein and astaxanthin, with antioxidant capacity, which can play a protective role in tissues. In this study, we produced and analyzed a C. vulgaris functional alcoholic beverage (produced using a traditional Brazilian alcoholic beverage, cachaça, and C. vulgaris biomass). Assays were conducted in vitro by radical scavenging tests, and in vivo, by modeling cortical spreading depression in rat brains. Scavenging radical assays showed that consumption of the C. vulgaris alcoholic beverage had a DPPH inhibition of 77.2%. This functional alcoholic beverage at a concentration of 12.5 g L-1 significantly improved cortical spreading depression velocity in the rat brains (2.89 mm min-1), when compared with cachaça alone (3.68 mm min-1) and control (distilled water; 3.25 mm min-1). Moreover, animals that consumed the functional beverage gained less weight than those that consumed just alcohol and the control groups. These findings suggest that the C. vulgaris functional alcoholic beverage plays a protective physiologic role in protecting brain cells from the effects of drinking ethanol.

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