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Migraine - Astrophysics Data System

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Last Updated: 22 May 2022

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Nonfunctional Na V 1.1 familial hemiplegic migraine mutant transformed into gain of function by partial rescue of folding defects

Mutations of SCN1A, a gene encoding the Na 1. 1 Na + channel, can result in familial migraine or epilepsy. Epileptogenic mutations cause impairment of its function, leading to decreased excitability of GABAergic neurons, but FHM-3 mutation studies have yielded contradictory results. Here we show that L1649Q function can be improved in environments that more closely mimic real neuron functioning.

Source link: https://ui.adsabs.harvard.edu/abs/2013PNAS..11017546C/abstract


Relating the cortical visual contrast gain response to spectroscopy-measured excitatory and inhibitory metabolites in people who experience migraine

The source of migraine symptoms have heightened visual cortical response amplitudes and contrast gain responses to high contrast flashering patterns in people with migraine, according to electrophysiological studies. Methods MRS-measured metabolite levels were obtained from 18 participants with migraine and 18 non-headache controls, respectively. Response functions were obtained on separate days from a subset of ten patients with migraine and 12 non-headache controls. Conclusions There were no significant differences in GABA and glutamate levels between groups nor checkerboard timepoint. In reaction to high-contrast flickering checkboards that distinguished those with migraine and without, there was no metabolic signature in visual cortex. Conclusion Our results show that the mechanisms behind contrast-flickering stimulus aversion are not largely explained by gross changes in metabolic activity in the primary visual cortex, according to our findings.

Source link: https://ui.adsabs.harvard.edu/abs/2022PLoSO..1766130C/abstract


Migraine patients visiting Chinese medicine hospital: Protocol for a prospective, registry-based, real-world observational cohort study

Migraine is a disabling, recurrent headache disease with ambiguous comorbidities. As an alternative or complementary treatment option for migraine in China, Chinese herbal medicine has been used as an alternative or complementary therapy approach for migraine. Randomised clinical trials focusing on internal validity, although with limited external validity, have the current evidence of the benefits of CHM for migraine relief. This real-world observational study aims to collect evidence of the effects and safety of CHM for migraine in the context of integrating Chinese medicine diagnostic procedures, patient preferences, and other topics that are relevant to clinical decision making. Effects of CHM will be assessed using a generalized estimated equation based on clinical outcome results. Discussion This report will present comprehensive evidence of CHM for migraine in the context of evidence-based practice.

Source link: https://ui.adsabs.harvard.edu/abs/2022PLoSO..1765137L/abstract


Defective membrane expression of the Na + -HCO 3 − cotransporter NBCe1 is associated with familial migraine

Many other heterozygous members of this family also suffered with glaucoma and migraine, with or without aura. Despite normal electrogenic activity in Xenopus oocytes, the 65bp mutant showed virtually no transport activity due to a predominant cytosolic retention in mammalian cells, with a predominant cytosolic retention. We found four additional migraine patients in a broader pRTA pedigree with different NBCe1 mutations, including four additional homozygous patients. The missing NBCe1 activity in astrocytes leads to migraines, according to the immunohistological and functional studies of these mutants.

Source link: https://ui.adsabs.harvard.edu/abs/2010PNAS..10715963S/abstract


Contribution of calcium-dependent facilitation to synaptic plasticity revealed by migraine mutations in the P/Q-type calcium channel

Remain calcium in presynaptic terminals can act via neuronal Ca 2+ sensor proteins in a model system, causing Ca 2+ -dependent facilitation of P/Q-type channels and short-term synaptic facilitation in a model system. We discover that gain-of-function mutations under Familial Hemiplegic Migraine type 1 occlude CDF of P/Q-type Ca 2+ channels in both exogenous and native versions of this article. In FHM-1 mutant mice, the change of P/Q-type channel CDF correlates with reduced short-term synaptic stimulation at cerebellar parallel fiber-to-Purkinje cell synapses. P/Q-type channels at parallel fiber terminals in FHM-1 mice, according to two-photon images, are in a basally facilitated state. Overall, the findings show that FHM-1 mutations directly affect both P/Q-type channel CDF and synaptic plasticity, which may possibly contribute to FHM-1's pathophysiology.

Source link: https://ui.adsabs.harvard.edu/abs/2010PNAS..10718694A/abstract

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions