Dose-dependent induction of mRNAs encoding brain-derived neurotrophic factor and heat-shock protein-72 after cortical spreading depression in the rat

Rangel, Yolanda; Karikó, Katalin; Harris, Valerie; Duvall, Monica E; Welsh, Frank A.

doi:10.1016/s0169-328x(01)00037-7

Cited by 18 publications

(22 citation statements)

References 36 publications

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“…Up-regulation of BDNF mRNA has been observed after cortical spreading depression in experimental in vivo studies [32, 33]. However, we did not find a difference in BDNF serum concentrations between patients with migraine with and without aura.…”

Section: Discussioncontrasting

confidence: 79%

Brain-derived neurotrophic factor in primary headaches

et al. 2012

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Brain derived neurotrophic factor (BDNF) is associated with pain modulation and central sensitization. Recently, a role of BDNF in migraine and cluster headache pathophysiology has been suspected due to its known interaction with calcitonin gene-related peptide. Bi-center prospective study was done enrolling four diagnostic groups: episodic migraine with and without aura, episodic cluster headache, frequent episodic tension-type headache, and healthy individuals. In migraineurs, venous blood samples were collected twice: outside and during migraine attacks prior to pain medication. In cluster headache patients serum samples were collected in and outside cluster bout. Analysis of BDNF was performed using enzyme-linked immunosorbent assay technique. Migraine patients revealed significantly higher BDNF serum levels during migraine attacks (n = 25) compared with headache-free intervals (n = 53, P < 0.01), patients with tension-type headache (n = 6, P < 0.05), and healthy controls (n = 22, P < 0.001). There was no significant difference between patients with migraine with aura compared with those without aura, neither during migraine attacks nor during headache-free periods. Cluster headache patients showed significantly higher BDNF concentrations inside (n = 42) and outside cluster bouts (n = 24) compared with healthy controls (P < 0.01, P < 0.05). BDNF is increased during migraine attacks, and in cluster headache, further supporting the involvement of BDNF in the pathophysiology of these primary headaches.

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Section: Discussioncontrasting

confidence: 79%

Brain-derived neurotrophic factor in primary headaches

et al. 2012

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“…The occurrence of CSD at later times is also unlikely because of the absence of changes in gene expression that are normally associated with CSD. Previous studies have shown that CSD triggers a robust elevation of c-fos mRNA in the ipsilateral cortex (Karikó et al, 1998;Rangel et al, 2001). In the present study, changes in c-fos mRNA or BDNF mRNA levels were not detected at 2 hours or 24 hours after application of 5-mol/L NaCl.…”

Section: Discussioncontrasting

confidence: 66%

“…Physiologic saline (0.15-mol/L NaCl) was applied in a similar fashion in controls (n ‫ס‬ 8). The occurrence of CSD was monitored through the thinned skull over the ipsilateral cortex (2 mm caudal to bregma, 4 mm lateral to the midline) using laser-Doppler flowmetry as described previously (Karikó et al, 1998;Rangel et al, 2001). …”

Section: Methodsmentioning

confidence: 99%

Induction of Tolerance to Focal Ischemia in Rat Brain: Dissociation between Cortical Lesioning and Spreading Depression

Muramatsu

Karikó

Welsh

2004

J Cereb Blood Flow Metab

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Summary: Cortical application of KCl has previously been shown to induce tolerance to a subsequent episode of cerebral ischemia. KCl triggers recurrent episodes of cortical spreading depression and produces a small lesion at the cortical application site. To determine whether a cortical lesion alone is sufficient to induce tolerance to ischemia, the authors used 5-mol/L NaCl to precondition rat brain 3 days before permanent occlusion of the middle cerebral artery. NaCl produced a small lesion at the application site without evoking cortical spreading depression. Preconditioning with 5-mol/L NaCl significantly attenuated the decrease in CBF after middle cerebral artery occlusion and reduced the volume of cortical infarction by 35%. The results show that a small cortical lesion, by itself, is sufficient to induce tolerance to ischemia.

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“…Immediately after cessation of CSD, BDNF mRNA levels increase 6-fold and return to baseline within 12 hours. In another model of CSD where the KCl concentration is lower, BDNF mRNA levels increase following a single or multiple CSD treatments [41]. In contrast, mRNA levels for basic fibroblastic growth factor, another protein with neuroprotective properties, increase by twelve hours and peak at 24 hours following CSD.…”

Section: Mechanisms Of Csdmentioning

confidence: 98%

Brain Adaptation to Stressful Stimuli: A New Perspective on Potential Therapeutic Approaches Based on BDNF and NMDA Receptors

Marini

Popolo²,

Pan³

et al. 2008

CNSNDDT

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A variety of sublethal or stressful stimuli induce a phenomenon in the brain known as tolerance, an adaptive response that protects the brain against the same stress, or against a different stress (cross-tolerance). Understanding the molecular mechanisms of brain preconditioning holds promise in developing innovative therapies to prevent and treat neurodegenerative disorders, particularly ischemic stroke. Many of the detailed steps involved in tolerance and cross-tolerance are unknown. It is also likely that different stressors differentially regulate sets of genes, transcription factors, and signal transduction pathways that depend upon the molecules that are released in response to the stressor, activation of particular receptors, and the surrounding milieu. The focus of this review is to highlight a few examples of stimuli that induce tolerance: 1) cortical spreading depression; 2) 3-nitropropionic acid; and 3) 2-deoxy-D-glucose. We will summarize by discussing one pathway where intracellular mediators may converge to upregulate intrinsic neuronal survival pathways to promote survival by resisting damage. This mechanism, activation of N-methyl-D-aspartate receptors and its integral relationship with brain-derived neurotrophic factor, may be a critical and general mechanism developed in brain to respond to stressful stimuli.

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Dose-dependent induction of mRNAs encoding brain-derived neurotrophic factor and heat-shock protein-72 after cortical spreading depression in the rat

Cited by 18 publications

References 36 publications

Brain-derived neurotrophic factor in primary headaches

Brain-derived neurotrophic factor in primary headaches

Induction of Tolerance to Focal Ischemia in Rat Brain: Dissociation between Cortical Lesioning and Spreading Depression

Brain Adaptation to Stressful Stimuli: A New Perspective on Potential Therapeutic Approaches Based on BDNF and NMDA Receptors

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