Spontaneous spreading depolarizations originate subcortically in a novel mouse model of familial hemiplegic migraine type 2.

The mechanisms of initiation of spreading depolarization (SD) are understudied due to a paucity of disease models with spontaneously occurring events. We here present a novel mouse model of familial hemiplegic migraine type 2 (FHM2), expressing the missense T345A-mutated α2 subunit of the Na/K adenosine triphosphatase pump (Atp1a2). Homozygous Atp1a2 mice showed regular spontaneous SDs that exhibit a diurnal rhythm and typically originate from the hippocampus.

On the Order and Orientation in Liquid Crystalline Polymer Membranes for Gas Separation.

To prevent greenhouse emissions into the atmosphere, separations like CO/CH and CO/N from natural gas, biogas, and flue gasses are crucial. Polymer membranes gained a key role in gas separations over the past decades, but these polymers are often not organized at a molecular level, which results in a trade-off between permeability and selectivity. In this work, the effect of molecular order and orientation in liquid crystals (LCs) polymer membranes for gas permeation is demonstrated.

Impaired θ-γ Coupling Indicates Inhibitory Dysfunction and Seizure Risk in a Dravet Syndrome Mouse Model.

Dravet syndrome (DS) is an epileptic encephalopathy that still lacks biomarkers for epileptogenesis and its treatment. Dysfunction of Na1.1 sodium channels, which are chiefly expressed in inhibitory interneurons, explains the epileptic phenotype.

Focal and generalized seizure activity after local hippocampal or cortical ablation of Na 1.1 channels in mice.

Early onset seizures are a hallmark of Dravet syndrome. Previous studies in rodent models have shown that the epileptic phenotype is caused by loss-of-function of voltage-gated Na 1.1 sodium channels, which are chiefly expressed in γ-aminobutyric acid (GABA)ergic neurons.

Apnea Associated with Brainstem Seizures in Mice Is Caused by Medullary Spreading Depolarization.

Seizure-related apnea is common and can be lethal. Its mechanisms however remain unclear and preventive strategies are lacking. We postulate that brainstem spreading depolarization (SD), previously associated with lethal seizures in animal models, initiates apnea upon invasion of brainstem respiratory centers.

Brainstem spreading depolarization and cortical dynamics during fatal seizures in Cacna1a S218L mice.

Sudden unexpected death in epilepsy (SUDEP) is a fatal complication of epilepsy in which brainstem spreading depolarization may play a pivotal role, as suggested by animal studies. However, patiotemporal details of spreading depolarization occurring in relation to fatal seizures have not been investigated. In addition, little is known about behavioural and neurophysiological features that may discriminate spontaneous fatal from non-fatal seizures.

Response characteristics of pruriceptive and nociceptive trigeminoparabrachial tract neurons in the rat.

We tested the possibility that the trigeminoparabrachial tract (VcPbT), a projection thought to be importantly involved in nociception, might also contribute to sensation of itch. In anesthetized rats, 47 antidromically identified VcPbT neurons with receptive fields involving the cheek were characterized for their responses to graded mechanical and thermal stimuli and intradermal injections of pruritogens (serotonin, chloroquine, and β-alanine), partial pruritogens (histamine and capsaicin), and an algogen (mustard oil). All pruriceptive VcPbT neurons were responsive to mechanical stimuli, and more than half were additionally responsive to thermal stimuli.