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Cortical spreading depression (CSD)-induced tolerance to transient focal cerebral ischemia in halothane anesthetized rats is affected by anesthetic level but not ATP-sensitive potassium channels.

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We investigated the participation of ATP-sensitive potassium (K(ATP)) channels, adenosine A1 receptors, and the effects of different levels of halothane anesthesia in the development of CSD-induced ischemic tolerance. To elicit CSD, 0.5 M KCl was applied for 2 h to the right hemisphere of halothane

Sensitivity to potassium tellurite of Escherichia coli cells deficient in CSD, CsdB and IscS cysteine desulfurases.

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The csdA, csdB and iscS genes encoding for cysteine desulfurase enzymatic activities in Escherichia coli were independently inactivated and potassium tellurite sensitivity, determined for each of the resulting mutant clones, was found to be iscS > csdB > csdA. Structural genes encoding for each of

TRESK: the lone ranger of two-pore domain potassium channels.

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TRESK (TWIK-related spinal cord K(+) channel, KCNK18) belongs to the two-pore domain (K2P) background (leak) potassium channel family. Unlike other K2P channels, TRESK is activated by the calcium signal in heterologous expression systems. The activation is mediated by the

Cortical Spreading Depolarization (CSD) Recorded from Intact Skin, from Surface of Dura Mater or Cortex: Comparison with Intracortical Recordings in the Neocortex of Adult Rats.

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In cerebral cortex of anesthetized rats single waves of spreading depolarization (CSD) were elicited by needle prick. CSD-related changes of DC (direct current) potentials were either recorded from the intact skin or together with concomitant changes of potassium concentration with

Migraine and Two-Pore-Domain Potassium Channels

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Migraine is a common, disabling neurological disorder with a genetic, environmental, and hormonal component with an annual prevalence estimated at ~15%. It is characterized by attacks of severe, usually unilateral and throbbing headache, and can be accompanied by nausea, vomiting, and photophobia.

Effect of potassium-induced cortical spreading depression on prostaglandin-induced fever in conscious and urethane-anesthetized rats.

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Potassium-induced cortical spreading depression (CSD) on prostaglandin E1 (PGE1) induced fever has been investigated in a dose-responsive experimental design in both conscious and urethane-anesthetized adult male Sprague-Dawley rats. While CSD in itself had no effect on nonfebrile body temperature

Clinical trials update from the American Heart Association meeting: ACORN-CSD, primary care trial of chronic disease management, PEACE, CREATE, SHIELD, A-HeFT, GEMINI, vitamin E meta-analysis, ESCAPE, CARP, and SCD-HeFT cost-effectiveness study.

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This article provides information and a commentary on landmark trials presented at the American Heart Association meeting held in November 2004, relevant to the pathophysiology, prevention, and treatment of heart failure. An open trial of the ACORN Cardiac Support Device (CSD) showed encouraging

Dissociation between CSD-Evoked Metabolic Perturbations and Meningeal Afferent Activation and Sensitization: Implications for Mechanisms of Migraine Headache Onset.

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The onset of the headache phase during attacks of migraine with aura, which occur in ∼30% of migraineurs, is believed to involve cortical spreading depression (CSD) and the ensuing activation and sensitization of primary afferent neurons that innervate the intracranial meninges, and their related

[Cortical spreading depression (CSD): a neurophysiological correlate of migraine aura].

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Cortical spreading depression (CSD) is a transient (60-120 s) and at 3-5 mm/min propagating depolarization wave of cortical neurons and glial cells and is characterized by a DC shift of 20-35 mV. It is accompanied by massive redistribution of ions between extracellular and intracellular compartments

Experimental Cortical Spreading Depression Induces NMDA Receptor Dependent Potassium Currents in Microglia.

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Cortical spreading depression (CSD) is a propagating event of neuronal depolarization, which is considered as the cellular correlate of the migraine aura. It is characterized by a change in the intrinsic optical signal and by a negative DC potential shift. Microglia are the resident macrophages of

Influence of MK-801 on brain extracellular calcium and potassium activities in severe hypoglycemia.

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The purpose of the present study was to examine the effect of blockade of N-methyl-D-aspartate (NMDA) receptors on the depolarization associated with severe hypoglycemia, which is commonly preceded by one or a few transient depolarizations reminiscent of cortical spreading depression (CSD). In the

Suppressive effect of chronic peroral topiramate on potassium-induced cortical spreading depression in rats.

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OBJECTIVE To evaluate the chronic effect of topiramate (TPM) on cortical spreading depression (CSD), which is thought to be related to migraine aura. METHODS Male rats (n = 30) were randomized to once-daily peroral treatment with TPM (50, 100, 200 or 600 mg/kg) or vehicle for 6 weeks. We evaluated

Integrated models of neurovascular coupling and BOLD signals: Responses for varying neural activations.

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A state-of-the-art integrated model of neurovascular coupling (NVC) (Dormanns et al., 2015b; Dormanns et al., 2016; Kenny et al., 2018) and the BOLD response (Mathias et al., 2017a; Mathias et al., 2017b) is presented with the ability to simulate the fMRI BOLD responses due to continuous neuronal

Differential neuromodulatory role of endocannabinoids in the rodent trigeminal sensory ganglion and cerebral cortex relevant to pain processing.

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Endocannabinoids are suggested to control pain, even though their clinical use is not fully validated and the underlying mechanisms are incompletely understood. To clarify the targets of endocannabinoid actions, we studied how activation of the endocannabinoid CB1 receptor (CB1R) affects neuronal

Depolarisation phenomena in traumatic and ischaemic brain injury.

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1. Cortical spreading depression is a non-physiological global depolarisation of neurones and astrocytes that can be initiated with varying degrees of difficulty in the normally perfused cerebral cortex in the experimental laboratory. Induction is typically with electrical stimulation, needling of

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