Cortical spreading depression and gene regulation: Relevance to migraine

Choudhuri, Rajani; Cui, Lisa; Yong, Chi; Bowyer, Susan M.; Klein, Robert M.; Welch, K. M. A.; Berman, Nancy E.J.

doi:10.1002/ana.10158

Cited by 87 publications

(28 citation statements)

References 48 publications

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“…There are numerous references in the literature to putative relationships between CSD and a variety of pathological states of the brain, including migraine with aura, 2, 10,19,23,36,43,44 stroke, 37 cerebral ischemia-infarctions, 19,20 and transient global amnesia. 19 As mentioned above, the relationship between CSD and MwA has been established.…”

Section: A Cortical Spreading Depression (Csd)mentioning

confidence: 99%

Mathematical approaches to modeling of cortical spreading depression

Miura

Huang

Wylie

2013

Chaos: An Interdisciplinary Journal of Nonlinear Science

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Migraine with aura (MwA) is a debilitating disease that afflicts about 25%-30% of migraine sufferers. During MwA, a visual illusion propagates in the visual field, then disappears, and is followed by a sustained headache. MwA was conjectured by Lashley to be related to some neurological phenomenon. A few years later, Leão observed electrophysiological waves in the brain that are now known as cortical spreading depression (CSD). CSD waves were soon conjectured to be the neurological phenomenon underlying MwA that had been suggested by Lashley. However, the confirmation of the link between MwA and CSD was not made until 2001 by Hadjikhani et al. [Proc. Natl. Acad. Sci. U.S.A. 98, 4687-4692 (2001)] using functional MRI techniques. Despite the fact that CSD has been studied continuously since its discovery in 1944, our detailed understandings of the interactions between the mechanisms underlying CSD waves have remained elusive. The connection between MwA and CSD makes the understanding of CSD even more compelling and urgent. In addition to all of the information gleaned from the many experimental studies on CSD since its discovery, mathematical modeling studies provide a general and in some sense more precise alternative method for exploring a variety of mechanisms, which may be important to develop a comprehensive picture of the diverse mechanisms leading to CSD wave instigation and propagation. Some of the mechanisms that are believed to be important include ion diffusion, membrane ionic currents, osmotic effects, spatial buffering, neurotransmitter substances, gap junctions, metabolic pumps, and synaptic connections. Discrete and continuum models of CSD consist of coupled nonlinear differential equations for the ion concentrations. In this review of the current quantitative understanding of CSD, we focus on these modeling paradigms and various mechanisms that are felt to be important for CSD.

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Section: A Cortical Spreading Depression (Csd)mentioning

confidence: 99%

Mathematical approaches to modeling of cortical spreading depression

Miura

Huang

Wylie

2013

Chaos: An Interdisciplinary Journal of Nonlinear Science

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“…Glutamate also increased lactate production by astroglia for utilization by neurons in metabolic activity [33, 34]. Neuronal inactivation by cortical spreading depression increased apolipoprotein E (apoE), a glial-derived protein [35]. Finally, progesterone inhibited neuronal excitability [36] and increased detection of GFAP immunoreactive processes at 1 h [9].…”

Section: Discussionmentioning

confidence: 99%

Neocortical and Hippocampal Glial Fibrillary Acidic Protein Immunoreactivity Shows Region-Specific Variation during the Mouse Estrous Cycle

Struble¹,

Afridi²,

Beckman-Randall³

et al. 2006

Neuroendocrinology

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Ovarian hormones modulate both neuronal and glial activation during the estrous cycle. These effects are particularly well characterized in the hypothalamus. Ovarian hormones also affect brain regions not directly related to reproductive function. In this study we used glial fibrillary acidic protein (GFAP) immunocytochemistry to quantify astroglial cells and process density in both the neocortex and hippocampus during the estrous cycle. Our data show that the density of GFAP immunoreactive processes in the hippocampus peaks on proestrus although cell density does not change. In contrast, both GFAP immunoreactive cell and process densities are elevated on diestrus and proestrus in the supragranular layer of the somatosensory cortex and reach a nadir on estrus and metestrus. This activation pattern is not apparent in the motor or cingulate cortex. Neocortical GFAP immunoreactivity appears to follow the distribution of estrogen receptor-α-like immunoreactivity. Our data show that ovarian hormones have regionally specific effects on glial activation within the neocortex. Characterizing glial activation by ovarian hormones is important since astroglia are the source of numerous trophic factors and play an important, although often unrecognized, role in neuronal metabolism and function.

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“…Therefore, a role for Ca V 2.1 channels could be dominant in the pathogenesis of migraine aura, indicating a potential molecular target for unspecific CCBs such as flunarizine. Alternatively, Ca V 1 channels (L-type) may also be involved, since they are upregulated in mouse brain subjected to episodes of CSD (Choudhuri et al, 2002). There are other targets, which could account for an action of CCBs (Reuter et al, 2002).…”

Section: Key Information About Clinical Usefulness Of Ccbsmentioning

confidence: 99%

Discovery and Development of Calcium Channel Blockers

2017

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In the mid 1960s, experimental work on molecules under screening as coronary dilators allowed the discovery of the mechanism of calcium entry blockade by drugs later named calcium channel blockers. This paper summarizes scientific research on these small molecules interacting directly with L-type voltage-operated calcium channels. It also reports on experimental approaches translated into understanding of their therapeutic actions. The importance of calcium in muscle contraction was discovered by Sidney Ringer who reported this fact in 1883. Interest in the intracellular role of calcium arose 60 years later out of Kamada (Japan) and Heibrunn (USA) experiments in the early 1940s. Studies on pharmacology of calcium function were initiated in the mid 1960s and their therapeutic applications globally occurred in the the 1980s. The first part of this report deals with basic pharmacology in the cardiovascular system particularly in isolated arteries. In the section entitled from calcium antagonists to calcium channel blockers, it is recalled that drugs of a series of diphenylpiperazines screened in vivo on coronary bed precontracted by angiotensin were initially named calcium antagonists on the basis of their effect in depolarized arteries contracted by calcium. Studies on arteries contracted by catecholamines showed that the vasorelaxation resulted from blockade of calcium entry. Radiochemical and electrophysiological studies performed with dihydropyridines allowed their cellular targets to be identified with L-type voltage-operated calcium channels. The modulated receptor theory helped the understanding of their variation in affinity dependent on arterial cell membrane potential and promoted the terminology calcium channel blocker (CCB) of which the various chemical families are introduced in the paper. In the section entitled tissue selectivity of CCBs, it is shown that characteristics of the drug, properties of the tissue, and of the stimuli are important factors of their action. The high sensitivity of hypertensive animals is explained by the partial depolarization of their arteries. It is noted that they are arteriolar dilators and that they cannot be simply considered as vasodilators. The second part of this report provides key information about clinical usefulness of CCBs. A section is devoted to the controversy on their safety closed by the Allhat trial (2002). Sections are dedicated to their effect in cardiac ischemia, in cardiac arrhythmias, in atherosclerosis, in hypertension, and its complications. CCBs appear as the most commonly used for the treatment of cardiovascular diseases. As far as hypertension is concerned, globally the prevalence in adults aged 25 years and over was around 40% in 2008. Usefulness of CCBs is discussed on the basis of large clinical trials. At therapeutic dosage, they reduce the elevated blood pressure of hypertensive patients but don't change blood pressure of normotensive subjects, as was observed in animals. Those active on both L- and T-type channels are efficient in nephropat...

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Cortical spreading depression and gene regulation: Relevance to migraine

Cited by 87 publications

References 48 publications

Mathematical approaches to modeling of cortical spreading depression

Mathematical approaches to modeling of cortical spreading depression

Neocortical and Hippocampal Glial Fibrillary Acidic Protein Immunoreactivity Shows Region-Specific Variation during the Mouse Estrous Cycle

Discovery and Development of Calcium Channel Blockers

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