Involvement of NMDA receptor subtypes in cortical spreading depression in rats assessed by fMRI

Shatillo, Artem; Salo, Raimo A.; Giniatullin, Rashid; Gröhn, Olli

doi:10.1016/j.neuropharm.2015.01.028

Cited by 43 publications

(35 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The functional association between SSD and NMDA receptors found in our studies is consistent with the “glutamate hypothesis,“ which suggests that this phenomenon is triggered by an intensive release of glutamate that activates postsynaptic NMDA receptors, thus evoking further neuronal firing and glutamate release.…”

Section: Discussionsupporting

confidence: 90%

“…This event also causes a significant increase of DA D1 receptor binding sites in the striatum, which further supports the involvement of the dopaminergic system in striatal SD (SSD). Moreover, the participation of ionotropic glutamate receptors, in particular N ‐methyl‐ d ‐aspartate (NMDA) receptors, to this phenomenon is confirmed by the block of SD by NMDA receptor antagonists . The interplay between NMDA and DA signaling in this phenomenon is indicated by the effects of local application of glutamate.…”

mentioning

confidence: 94%

See 1 more Smart Citation

Striatal spreading depolarization: Possible implication in levodopa‐induced dyskinetic‐like behavior

et al. 2019

View full text Add to dashboard Cite

A BS TRACT: Objective: Spreading depolarization (SD) is a transient self-propagating wave of neuronal and glial depolarization coupled with large membrane ionic changes and a subsequent depression of neuronal activity. Spreading depolarization in the cortex is implicated in migraine, stroke, and epilepsy. Conversely, spreading depolarization in the striatum, a brain structure deeply involved in motor control and in Parkinson's disease (PD) pathophysiology, has been poorly investigated. Methods: We characterized the participation of glutamatergic and dopaminergic transmission in the induction of striatal spreading depolarization by using a novel approach combining optical imaging, measurements of endogenous DA levels, and pharmacological and molecular analyses.Results: We found that striatal spreading depolarization requires the concomitant activation of D1-like DA and Nmethyl-D-aspartate receptors, and it is reduced in experimental PD. Chronic L-dopa treatment, inducing dyskinesia in the parkinsonian condition, increases the occurrence and speed of propagation of striatal spreading depolarization, which has a direct impact on one of the signaling pathways downstream from the activation of D1 receptors. Conclusion: Striatal spreading depolarization might contribute to abnormal basal ganglia activity in the dyskinetic condition and represents a possible therapeutic target.

show abstract

Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 94%

Striatal spreading depolarization: Possible implication in levodopa‐induced dyskinetic‐like behavior

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In the rat-model, both ketamine and the non-specific NMDA antagonist, MK-801 have been shown to block CSD, demonstrated electrophysiologically and by fMRI [29]. In a double-blinded, randomized parallel-group controlled study of 18 patients with migraine with aura, Afridi et al tested the effect of intranasal ketamine compared to midazolam on aura.…”

Section: Discussionmentioning

confidence: 99%

Intravenous ketamine for subacute treatment of refractory chronic migraine: a case series

et al. 2016

View full text Add to dashboard Cite

BackgroundRefractory migraine is a challenging condition with great impact on health related quality of life. Intravenous (IV) ketamine has been previously used to treat various refractory pain conditions. We present a series of patients with refractory migraine treated with intravenous ketamine in the hospital setting.MethodsBased on retrospective chart review, we identified six patients with refractory migraine admitted from 2010 through 2014 for treatment with intravenous ketamine. Ketamine was administered using a standard protocol starting with a dose of 0.1 mg/kg/hr and increased by 0.1 mg/kg/hr every 3 to 4 h as tolerated until the target pain score of 3/10 was achieved and maintained for at least 8 h. Visual Analogue Scale (VAS) scores at time of hospital admission were obtained as well as average baseline VAS scores prior to ketamine infusion. A phone interview was conducted for follow-up of migraine response in the 3 to 6 months following ketamine infusion.ResultsThe study sample had a median age of 36.5 years (range 29–54) and 83% were women. Pre-treatment pain scores ranged from 9 to 10. All patients achieved a target pain level of 3 or less for 8 h; the average ketamine infusion rate at target was 0.34 mg/kg/hour (range 0.12–0.42 mg/kg/hr). One patient reported a transient out-of-body hallucination following an increase in the infusion rate, which resolved after decreasing the rate. There were no other significant side effects.ConclusionIV ketamine was safely administered in the hospital setting to patients with refractory chronic migraine. Treatment was associated with short term improvement in pain severity in 6 of 6 patients with refractory chronic migraine. Prospective placebo-controlled trials are needed to assess short term and long-term efficacy of IV ketamine in refractory chronic migraine.Electronic supplementary materialThe online version of this article (doi:10.1186/s10194-016-0700-3) contains supplementary material, which is available to authorized users.

show abstract

“…Agonist of glutamate receptors can trigger CSD [67], while the non-competitive NMDA antagonist MK 801 is able to suppress the formation of cortical CSD waves [68]. Recent data suggest that different subtypes of NMDA receptors may play diverse roles in the formation of CSD, thus subtype specific antagonist may provide a therapeutic approach against CSD [69].…”

Section: Auramentioning

confidence: 99%

Tryptophan Catabolites and Migraine

Bohár

Párdutz

Vécsei

2016

CPD

View full text Add to dashboard Cite

Abstract:Migraine is a highly disabling neurological condition affecting around 15% of the population worldwide.Decades of intensive research shed some light on diseases pathomechanism, but information is still missing about the initiation of the attack. In the past century, serotonin emerged as the main target of both basic and therapeutic research. As a result, the triptans, the only approved migraine specific drugs were developed. The involvement of glutamatergic mechanism in migraine headache development such as cortical hyperexcitability, and cortical spreading depression as the pathological correlate of migraine aura called the attention to the kynurenine pathway in migraine pathomechanism. The serotonin and kynurenine pathways are closely connected, as they both are the metabolic routes of the amino acid tryptophan. Kynurenine catabolites are important participants in glutamatergic neurotransmission, regulation also nociceptive processing of the trigeminal system. The current work attempts to collect recent data on both serotonin and kynurenine research related to migraine and emphasizes the importance of further research on this topic.

show abstract

Involvement of NMDA receptor subtypes in cortical spreading depression in rats assessed by fMRI

Cited by 43 publications

References 60 publications

Striatal spreading depolarization: Possible implication in levodopa‐induced dyskinetic‐like behavior

Striatal spreading depolarization: Possible implication in levodopa‐induced dyskinetic‐like behavior

Intravenous ketamine for subacute treatment of refractory chronic migraine: a case series

Tryptophan Catabolites and Migraine

Contact Info

Product

Resources

About