A delayed class of BOLD waveforms associated with spreading depression in the feline cerebral cortex can be detected and characterised using independent component analysis (ICA)

Netsiri, Chaiyapoj; Bradley, Daniel P.; Takeda, Tsunehiro; Smith, M. Paul; Papadakis, N.; Hall, Laurance D.; Parsons, Andrew A.; James, Michael F.; Huang, Christopher L.‐H.

doi:10.1016/s0730-725x(03)00199-1

Cited by 13 publications

(6 citation statements)

References 52 publications

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“…Thus, our results provide evidence to suggest that tonabersat should be able to prevent peripheral sensitization within the trigeminal ganglion. Interestingly, in other studies relevant to migraine pathology, tonabersat was shown to block plasma protein extravasation following trigeminal nerve stimulation and to inhibit cortical spreading depression and nitric oxide release 26,44‐46 . In addition, tonabersat was shown to block trigeminal parasympathetic reflexes, which are involved in migraine and rhinosinusitis 4,35 .…”

Section: Discussionmentioning

confidence: 95%

“…Interestingly, in other studies relevant to migraine pathology, tonabersat was shown to block plasma protein extravasation following trigeminal nerve stimulation and to inhibit cortical spreading depression and nitric oxide release. 26,[44][45][46] In addition, tonabersat was shown to block trigeminal parasympathetic reflexes, which are involved in migraine and rhinosinusitis. 4,35 Whether tonabersat's ability to block gap junction signaling in the trigeminal ganglion is involved in mediating any of these inhibitory effects remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

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Tonabersat Inhibits Trigeminal Ganglion Neuronal‐Satellite Glial Cell Signaling

et al. 2009

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Background Sensitization and activation of trigeminal neurons are implicated in the underlying pathology of migraine, acute sinusitis, and allergic rhinitis. Cell bodies of trigeminal neurons that provide sensory innervation of the dura and nasal mucosa reside in the trigeminal ganglion in association with satellite glial cells where they communicate via gap junctions. Gap junctions, channels formed by connexins, modulate the excitability state of both neurons and glia under pathological conditions. Tonabersat, a compound being tested as an antimigraine drug, is thought to block gap junction activity. Objective To investigate the cellular events within trigeminal ganglia that may account for the significant comorbidity of migraine and rhinosinusitis and determine the effect of tonabersat on neuron-satellite glia communication. Methods Sprague Dawley rats injected with True Blue were used to localize neuronal cell bodies in the ganglion and study neuronglia signaling via gap junctions in the trigeminal ganglion. Dye coupling studies were conducted under basal conditions and in response to tumor necrosis factor-alpha injection into the whisker pad and/or capsaicin injection into the eyebrow. Changes in connexin 26 and active p38 levels were determined by immunohistochemistry. In addition, the effect of tonabersat prior to chemical stimulation on gap junction activity and expression of connexins and active p38 was investigated. Results Injection of tumor necrosis factor-alpha, a cytokine implicated in the pathology of acute sinusitis and allergic rhinitis, into the V2 region was shown to lower the amount of capsaicin required to stimulate neurons located in the V1 region of the ganglion. While injection of tumor necrosis factor-alpha into the whisker pad or capsaicin injection into the eyebrow alone did not cause increased dye movement, the combination of both stimuli greatly increased neuron-satellite glia communication via gap junctions in both V1 and V2 regions. The change in gap junction activity was accompanied by increased expression of connexin 26 and active p38 levels in both neurons and satellite glia in V1 and V2 regions. Pretreatment with tonabersat inhibited gap junction communication between neurons and satellite glia and blocked the increase in connexin 26 and active p38 levels in response to injection of both tumor necrosis factor-alpha (V2) and capsaicin (V1). Conclusions We propose that increased levels of tumor necrosis factor-alpha, as reported during acute sinusitis and allergic rhinitis, reduces the amount of capsaicin necessary to stimulate V1 neurons that leads to cellular changes in both V1 and V2 regions. The cellular events observed in this study may help to explain, in part, the significant comorbidity reported with migraine and rhinosinusitis. In addition, we have provided evidence to suggest that tonabersat can prevent increased neuron-satellite glia signaling and, thus, may be useful in the treatment of migraine, acute sinusitis, and allergic rhinitis.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Tonabersat Inhibits Trigeminal Ganglion Neuronal‐Satellite Glial Cell Signaling

et al. 2009

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“…Independent component analysis (ICA) was used as an exploratory data analysis technique to separate signals from individual pixels across whole BOLD data sets into component signals (Netsiri et al, 2003). Independent component analysis (ICA) was used as an exploratory data analysis technique to separate signals from individual pixels across whole BOLD data sets into component signals (Netsiri et al, 2003).…”

Section: Vascular Phenomena Associated With Csdmentioning

confidence: 99%

Physiological studies of cortical spreading depression

et al. 2007

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Cortical spreading depression (CSD) produces propagating waves of transient neuronal hyperexcitability followed by depression. CSD is initiated by K + release following neuronal firing or electrical, mechanical or chemical stimuli. A triphasic (30-50 s) cortical potential transient accompanies localized transmembrane redistributions of K + , glutamate, Ca 2+ , Na + , Cl x and H + . Accumulated K + in the restricted interstitial space can cause both further neuronal depolarisation and inward movement of K + into astrocytes that buffers this increased extracellular K + concentration ([K + ]) o . However, astrocyte interconnections may then propagate the CSD wave by K + liberation through an opening of remote K + channels by volume, Ca 2+ or N-methyl-Daspartate receptor activation. Changes in cerebral blood volume and in apparent water diffusion co-efficient (ADC) accompanying CSD were first studied using magnetic resonance imaging (MRI) in whole lissencephalic brains. Diffusion-weighted echoplanar imaging in gyrencephalic brains went on to demonstrate CSD features that paralleled classical migraine aura. The ADC activity persisted minutes/hours post KCl stimulus. Pixelwise analyses distinguished single primary events and multiple, spatially restricted, slower propagating, secondary events whose detailed features varied with the nature of the originating stimulus. These ADC changes varied reciprocally with T2*-weighted (i.e. referring to spin-spin relaxation times) waveforms reflecting local blood flow. There followed prolonged decreases in cerebral blood flow culminating in late cerebrovascular changes blocked by the antimigraine agent sumatriptan. CSD phenomena have possible translational significance for human migraine aura and other cerebral pathologies such as the peri-infarct depolarisation events that follow ischaemia and brain injury.

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“…6 Direct evidence of CSD during aura in patients is still lacking, but previous studies have shown changes in regional cerebral blood flow corresponding to those seen in animals during CSD using planar xenon, 7 single photon emission computed tomography (SPECT), 8 and positron emission tomography (PET). 10,11 One study using BOLD fMRI reported signal changes with several characteristics of CSD during a typical scintillating scotoma in a migraine patient provoked by physical activity. 10,11 One study using BOLD fMRI reported signal changes with several characteristics of CSD during a typical scintillating scotoma in a migraine patient provoked by physical activity.…”

mentioning

confidence: 99%

“…9 Detection of CSD waves by blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) has been validated in vivo in the feline brain. 10,11 One study using BOLD fMRI reported signal changes with several characteristics of CSD during a typical scintillating scotoma in a migraine patient provoked by physical activity. 12 Similar fMRI studies during migraine aura has not been performed, probably because migraine aura is notoriously difficult to study due to the unpredictable and shortlasting nature of attacks, and because no efficient and consistent method for experimental aura provocation has been developed.…”

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confidence: 99%