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A propofol binding site in the voltage sensor domain mediates inhibition of HCN1 channel activity.
Sci Adv
January 2025
Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Hyperpolarization-activated and cyclic nucleotide-gated (HCN) ion channels are members of the cyclic nucleotide-binding family and are crucial for regulating cellular automaticity in many excitable cells. HCN channel activation contributes to pain perception, and propofol, a widely used anesthetic, acts as an analgesic by inhibiting the voltage-dependent activity of HCN channels. However, the molecular determinants of propofol action on HCN channels remain unknown.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Arizona, Tucson, AZ, USA.
Background: Cerebral microvascular dysfunction and nitro-oxidative stress are present in patients with Alzheimer's disease (AD) and may contribute to disease progression and severity. A pro-nitro-oxidative environment can lead to post-translational modifications of ion channels central to microvascular regulation in the brain, including the large conductance Ca-activated K channels (BK). Nitro-oxidative modulation of BK can resulting in decreased activity and vascular hyper-contractility, thus compromising neurovascular regulation.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Yale University School of Medicine, New Haven, CT, USA.
Background: In neurodegenerative disease such as Alzheimer's disease and stroke, the brain transitions to pro-inflammatory profile, where microglia and T-cells in the brain have increase inflammatory profiles, along with increased Kv1.3 potassium channel abundance. Pharmacological blockade of Kv1.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Indiana University, Bloomington, IN, USA.
Background: The roles of Aβ in the pathogenesis of Alzheimer 's disease (AD) include disruption of synaptic communication/function and synaptic plasticity mechanisms thought to underlie learning and memory. Exactly how these abnormal processes arise is incompletely understood, but evidence suggests that dysregulation of intracellular Ca levels is involved in alterations of neuronal excitability, synaptic remodeling, and neurodegeneration in AD. Our lab has focused on the potential involvement of voltage-gated potassium channels (VGKCs) in these processes, particularly Kv1.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Yale University School of Medicine, New Haven, CT, USA.
Background: Kv1.3 channels are promising therapeutic targets to modulate neuroinflammatory responses in neurodegenerative disease including Alzheimer's disease (AD). Although the ability of Kv1.
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