Cortical spreading depression activates and upregulates MMP-9

Gürsoy‐Özdemir, Yasemin; Qiu, Jianhua; Matsuoka, Norihiro; Bolay, Hayrünnisa; Bermpohl, Daniela; Jin, Hongwei; Wang, Xiaoying; Rosenberg, Gary A.; Lo, Eng H.; Moskowitz, Michael A.

doi:10.1172/jci21227

Cited by 259 publications

(213 citation statements)

References 58 publications

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“…In support of this view, Kapural et al (2002) measured S100B and NSE levels in patients with primary central nervous system lymphoma who underwent iatrogenic BBB disruption by intra-arterial mannitol infusion, and found that serum levels of S100B increased while NSE levels remained constant after disruption of the BBB. It has been suggested that activation of matrix metalloproteinases might cause BBB disruption during a migraine attack (Gursoy-Ozdemir et al 2004). In accordance, Teepker et al reported elevated S100B levels in migraine patients both during and after an attack, and concluded that this was the result of a prolonged BBB disruption in migraine (Teepker et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

et al. 2011

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Although migraine has mainly been considered as a benign disease, there is cumulative evidence of silent changes in the brain, brainstem, or cerebellum and subtle subclinical cerebellar dysfunction. In this study, in order to investigate a possible neuronal and/or glial damage at the cellular level in migraine, we measured and compared serum levels of S100B which is a protein marker of glial damage or activation, and neuron specific enolase (NSE) which is a marker of neuronal damage, in migraine patients and control subjects. Serum levels of S100B and NSE were measured in blood samples from 41 patients with migraine-without aura taken during a migraine attack (ictal) and in the attack-free period between migraine attacks (interictal) and 35 age- and sex-matched controls. Patients with migraine-without aura had significantly higher ictal serum levels of S100B and NSE (P < 0.05, for both) than control subjects; whereas in the interictal phase, there was a significant increment only in S100B levels (P < 0.05) compared to controls. On the other hand, serum levels of S100B and NSE in ictal and interictal blood samples did not differ significantly. The findings of increased ictal serum S100B and NSE levels together with increased interictal levels of S100B suggested that migraine might be associated with glial and/or neuronal damage in the brain and a prolonged disruption of blood-brain barrier. Increased interictal serum levels of S100B might point out to an insidious and slow damaging process in migraine patients.

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Section: Discussionmentioning

confidence: 99%

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

et al. 2011

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“…Activated microglia migrate to lesion foci and release matrix metalloproteinases and cytokines. In particular, metalloproteinase release and activation cause BBB impairment by degrading the basal lamina (Gursoy-Ozdemir et al 2004;Gurney et al 2006). BBB disruption provokes the immediate and focal activation of microglia (Nimmerjahn et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Detachment of Brain Pericytes from the Basal Lamina is Involved in Disruption of the Blood–Brain Barrier Caused by Lipopolysaccharide-Induced Sepsis in Mice

et al. 2008

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The blood-brain barrier (BBB) is highly restrictive of the transport of substances between blood and the central nervous system. Brain pericytes are one of the important cellular constituents of the BBB and are multifunctional, polymorphic cells that lie within the microvessel basal lamina. The present study aimed to evaluate the role of pericytes in the mediation of BBB disruption using a lipopolysaccharide (LPS)-induced model of septic encephalopathy in mice. ICR mice were injected intraperitoneally with LPS or saline and were sacrificed at 1, 3, 6, and 24 h after injection. Sodium fluorescein accumulated with time in the hippocampus after LPS injection; this hyperpermeability was supported by detecting the extravasation of fibrinogen. Microglia were activated and the number of microglia increased with time after LPS injection. LPS-treated mice exhibited a broken basal lamina and pericyte detachment from the basal lamina at 6-24 h after LPS injection. The disorganization in the pericyte and basal lamina unit was well correlated with increased microglial activation and increased cerebrovascular permeability in LPS-treated mice. These findings suggest that pericyte detachment and microglial activation may be involved in the mediation of BBB disruption due to inflammatory responses in the damaged brain.

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“…We also detected that CSD resulted in MMP 9 activation in cerebral cortex and pia-glial barriers, decreases in laminin and other markers of intact compartmental barriers and BBB disruption (Gursoy-Ozdemir et al 2004). Thereby, vasoactive and nociceptive substances released from brain parenchyma could reach and activate perivascular trigeminal nerve endings.…”

Section: Cortical Spreading Depression Waves Activate Trigeminal Nervementioning

confidence: 72%

The first phase of a migraine attack resides in the cortex

Bolay

2012

J Neural Transm

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Migraine headache is generated by the complex interaction of various players such as genetic predisposition, environmental triggers and intrinsic factors. The initial mechanism of a migraine attack has long been a controversial topic and exploring its origin is a challenging task. The scientific evidences so far indicate neuronal dysfunction in the cerebral cortex and particularly cortical spreading depression waves, as upstream to cascade of events leading to a migraine attack. Neocortex, evolutionary valuable part of the brain, is surrounded by pain sensing system that is finely tuned for detecting noxious signals. Abnormal functioning of more than one cortical area in migraineurs may suggest that hyperexcitable neocortex could be more easily challenged, overreacts and depolarize to repetitive sensorial stimuli and could switch to extreme excitability state where spreading depression waves occur. In this paper, I will review the data supporting the notion that migraine is a neuronal disorder where cortex has prime importance. Despite clear demonstration of cortical participation in migraine, the contribution of brain structures other than cortex to the development of migraine remains unclear.

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Cortical spreading depression activates and upregulates MMP-9

Cited by 259 publications

References 58 publications

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

Detachment of Brain Pericytes from the Basal Lamina is Involved in Disruption of the Blood–Brain Barrier Caused by Lipopolysaccharide-Induced Sepsis in Mice

The first phase of a migraine attack resides in the cortex

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