Cortical spreading depression affects Fos expression in the hypothalamic paraventricular nucleus and the cerebral cortex of both hemispheres

Chowdhury, Golam M. I.; Liu, Ying; Tanaka, Masuo; Fujioka, Takashi; Ishikawa, Ai; Nakamura, Shôji

doi:10.1016/s0168-0102(02)00207-9

Cited by 11 publications

(5 citation statements)

References 30 publications

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“…Unilateral SD can induce bilateral activation of brain regions relevant for pain. For example, unilateral SD increased c‐fos expression bilaterally in periaqueductal gray 45 and paraventricular hypothalamus 46 . Indeed, migraine‐associated cutaneous allodynia develops in a stepwise fashion with progressive sensitization of higher order (eg, bilateral) neuronal populations 47 .…”

Section: Discussionmentioning

confidence: 99%

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Harriott

Chung

Uner

et al. 2020

Annals of Neurology

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Objective Cortical spreading depression (SD) is an intense depolarization underlying migraine aura. Despite the weight of evidence linking SD to the pain phase of migraine, controversy remains over a causal role of SD in cephalgia because of the invasive nature of previous SD induction methods. To overcome this problem, we used a novel minimally invasive optogenetic SD induction method and examined the effect of SD on behavior. Methods Optogenetic SD was induced as a single event or repeatedly every other day for 2 weeks. End points, including periorbital and hindpaw mechanical allodynia, mouse grimace, anxiety, and working memory, were examined in male and female mice. Results A single SD produced bilateral periorbital mechanical allodynia that developed within 1 hour and resolved within 2 days. Sumatriptan prevented periorbital allodynia when administered immediately after SD. Repeated SDs also produced bilateral periorbital allodynia that lasted 4 days and resolved within 2 weeks after the last SD. In contrast, the hindpaw withdrawal thresholds did not change after repeated SDs suggesting that SD‐induced allodynia was limited to the trigeminal region. Moreover, repeated SDs increased mouse grimace scores 2 days after the last SD, whereas a single SD did not. Repeated SDs also increased thigmotaxis scores as a measure of anxiety. In contrast, neither single nor repeated SDs affected visuospatial working memory. We did not detect sexual dimorphism in any end point. Interpretation Altogether, these data show a clinically congruent causal relationship among SD, trigeminal pain, and anxiety behavior, possibly reflecting SD modulation of hypothalamic, thalamic, and limbic mechanisms. ANN NEUROL 2021;89:99–110

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Section: Discussionmentioning

confidence: 99%

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Harriott

Chung

Uner

et al. 2020

Annals of Neurology

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“…CSD may directly modulate the hypothalamus, thus a connection between CSD/aura and CH. Iqbal Chowdhury et al [15] noted elevation in cFos levels in the magnocellular region of the hypothalamic paraventricular nucleus after induction of CSD. The paraventricular nucleus also is modulated by orexin [16].…”

Section: Aura Pathogenesis In Cluster Headachementioning

confidence: 99%

Cluster Headache with Aura

Rozen¹

2010

Curr Pain Headache Rep

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Aura was not recognized as a clinical symptom of cluster headache until fairly recently, but studies now have indicated that upwards of 20% of patients with cluster headache may have aura, the same percentage of migraine sufferers who have aura. This paper looks at the epidemiology of cluster headache with aura, suggests possible roles of cortical spreading depression in cluster headache pathogenesis, and looks at the clinical/diagnostic implications of aura in cluster headache sufferers.

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“…Fos expression is increased specifically in the magnocellular region of the hypothalamic paraventricular nucleus (PVN) and by the same way, in the ipsilateral cortex, whereas decreased Fos expression is noted in both the parvocellular region of the PVN and in the entire cortex contralateral to the CSD site (Iqbal Chowdhury et al, 2003). Consistent with reduced Fos expression, approximately 40% of neurons in the contralateral cortex show suppressed electrical activity during CSD, suggesting that the CSD can affect Fos expression in distinct areas.…”

Section: Discussionmentioning

confidence: 99%

Stereological Analysis of Early Gene Expression Using Egr-1 Immunolabeling After Spreading Depression in the Rat Somatosensory Cortex

et al. 2019

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Early growth response-1 (Egr-1), defined as a zinc finger transcription factor, is an upstream master switch of the inflammatory response, and its expression can be used to investigate the spatial and temporal extent of inflammatory changes in the brain. Cortical spreading depression (CSD) is characterized as a slowly propagating (2–5 mm/min) depolarization wave through neurons and astrocytes in humans that contributes to migraines and possibly to other brain pathologies. In rodents, CSD can be induced experimentally, which involves unilateral depolarization that is associated with microglial and astrocyte responses. The impact of CSD on structures beyond the affected hemisphere has not been explored. Here, we used an optical fractionator method to investigate potential correlations between the number of and period of the eletrophysiologic record of CSD phenomena and Egr-1 expression in ipsilateral and contralateral hemispheres. CSD was elicited by the restricted application of a 2% KCl solution over the left premotor cortex. Electrophysiological events were recorded using a pair of Ag/AgCl agar-Ringer electrodes for 2 or 6 h. An optical fractionator was applied to count the Egr-1 positive cells. We found that CSD increased Egr-1 expression in a time- and event-dependent manner in the ipsilateral/left hemisphere. Although CSD did not cross the midline, multiple CSD inductions were associated with an increased number of Egr-1 positive cells in the contralateral/right hemisphere. Thus, repeated CSD waves may have far reaching effects that are more global than previously considered possible. The mechanism of contralateral expression is unknown, but we speculate that callosal projections from the depolarized hemisphere may be related to this phenomenon.

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Cortical spreading depression affects Fos expression in the hypothalamic paraventricular nucleus and the cerebral cortex of both hemispheres

Cited by 11 publications

References 30 publications

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Cluster Headache with Aura

Stereological Analysis of Early Gene Expression Using Egr-1 Immunolabeling After Spreading Depression in the Rat Somatosensory Cortex

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