1. KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached patch recording. 2. Stimulation of M1 receptors by 10 microM oxotremorine-M (Oxo-M) strongly reduced (to 0-10%) currents produced by KCNQ1-4 subunits expressed individually and also those produced by KCNQ2 + KCNQ3 and KCNQ1 + KCNE1 heteromers, which are thought to generate neuronal M-currents (IK,M) and cardiac slow delayed rectifier currents (IK,s), respectively. 3. The activity of KCNQ2 + KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced by Oxo-M applied to the extra-patch membrane. 4. It is concluded that M1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2 + KCNQ3 channels, like that of native M-channels, requires a diffusible second messenger.
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http://dx.doi.org/10.1111/j.1469-7793.2000.t01-2-00349.x | DOI Listing |
Elife
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Department of Neurology, Baylor College of Medicine, Houston, United States.
Neurobiol Dis
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The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria 3052, Australia. Electronic address:
Background: Developmental and epileptic encephalopathies (DEE) are rare but severe neurodevelopmental disorders characterised by early-onset seizures often combined with developmental delay, behavioural and cognitive deficits. Treatment for DEEs is currently limited to seizure control and provides no benefits to the patients' developmental and cognitive outcomes. Genetic variants are the most common cause of DEE with KCNQ2 being one of the most frequently identified disease-causing genes.
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Department of Neuroscience, Section of Pharmacology, University of Naples Federico II, Naples 80131, Italy.
Pathogenic variants in encoding Kv7.2 voltage-gated potassium channel subunits cause developmental encephalopathies (-encephalopathies), both with and without epilepsy. We herein describe the clinical, in vitro, and in silico features of two encephalopathy-causing variants (A317T, L318V) in Kv7.
View Article and Find Full Text PDFBiochim Biophys Acta Biomembr
January 2025
Graduate School of Medicine, Osaka University, Japan; Graduate School of Frontier Biosciences, Osaka University, Japan.
Phosphatidylinositol 4,5-bisphosphate (PIP) is a key membrane lipid regulating various ion channel activities. Currently, several molecular tools are used to modulate PIP levels, each of which has distinct advantages and drawbacks. In this study, we proposed a novel methodology using heterologous Xenopus oocytes to precisely manipulate PIP levels using phospholipase C (PLC)-ζ, which hydrolyzes PIP.
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Department of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, China.
Recent advances in exome and targeted sequencing have significantly improved the aetiological diagnosis of epilepsy, revealing an increasing number of epilepsy-related pathogenic genes. As a result, the diagnosis and treatment of epilepsy have become more accessible and more traceable. Voltage-gated potassium channels (Kv) regulate electrical excitability in neuron systems.
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