The action of propofol on voltage-gated calcium channels was investigated in cultured dorsal root ganglion neurons from chick embryos. The Ca2+ current was measured by using the patch-clamp technique in whole cell configuration. Low-voltage-activated (LVA) and high-voltage-activated (HVA) Ca2+ currents were selected by means of appropriate stimulation protocols. Propofol (0.3 mM) inhibited the LVA T-type current by 80% (P < 0.001). The same concentration of propofol reduced the HVA Ca2+ current with a high variability (10%-75%). The inactivation time constant of the HVA current was also shortened to 50% by propofol. omega-Conotoxin and nifedipine were used to discriminate between the HVA N- and L-type current components. Only the L-type component was strongly depressed (75%) by propofol (P < 0.001); different effects on the HVA current might, therefore, reflect different percentages of L- and N-type channels in neurons. We conclude that propofol inhibits the T-type and L-type components of the Ca2+ current. This inhibition may play a role in the cardiovascular side effects clinically observed.
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http://dx.doi.org/10.1213/00000539-199405000-00021 | DOI Listing |
Angew Chem Int Ed Engl
January 2025
East China Normal University, Dept. of Chemistry, Dongchuan Road 500, 200062, Shanghai, CHINA.
Monitoring dynamic neurochemical signals in the brain of free-moving animals remains great challenging in biocompatibility and direct implantation capability of current electrodes. Here we created a self-supporting polymer-based flexible microelectrode (rGPF) with sufficient bending stiffness for direct brain implantation without extra devices, but demonstrating low Young's modulus with remarkable biocompatibility and minimal position shifts. Meanwhile, screening by density functional theory (DFT) calculation, we designed and synthesized specific ligands targeting Mg2+ and Ca2+, and constructed Mg-E and Ca-E sensors with high selectivity, good reversibility, and fast response time, successfully monitoring Mg2+ and Ca2+ in vivo up to 90 days.
View Article and Find Full Text PDFPflugers Arch
January 2025
Laboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center of RAS, 2/31 Lobachevsky St, Kazan, 420111, RT, Russia.
Many synaptic vesicles undergo exocytosis in motor nerve terminals during neuromuscular communication. Endocytosis then recovers the synaptic vesicle pool and presynaptic membrane area. The kinetics of endocytosis may shape neuromuscular transmission, determining its long-term reliability.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Alzheimer's disease (AD) is the most frequent cause of dementia. Since there are complex pathophysiological mechanisms behind AD, and there is no effective treatment strategy, it is necessary to introduce novel multi-targeting agents with fewer side effects and higher efficacy. Polydatin (PD) is a naturally occurring resveratrol glucoside employing multiple mechanisms toward neuroprotection.
View Article and Find Full Text PDFEur J Neurol
January 2025
Department of Pharmacotherapy, University of Utah Health, Salt Lake City, Utah, USA.
Background: Reduction of intracellular Na accumulation through late Na current inhibition has been recognized as a target for cardiac Ca handling which underlies myocardial contractility and relaxation in heart failure (HF). Riluzole, an Na channel blocker with enhancement of Ca-activated K channel function, used for management of amyotrophic lateral sclerosis (ALS), is effective in suppressing Ca leak and therefore may improve cardiac function.
Objectives: The study aim was to investigate whether riluzole lowers HF incidence.
Alzheimers Dement
December 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Background: The hippocampus, a region vital for memory and cognition, is prone to abnormal deposition of beta-amyloid (Aβ) during the early stages of the Alzheimer's disease. Aβ-associated pathophysiological mechanisms instigate dendritic deficit, neuronal loss, and neuroinflammation, leading to abnormal functional and behavioral changes. These factors directly impact tissue microstructures.
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