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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269765PMC
http://dx.doi.org/10.1111/j.1469-7793.2000.t01-2-00349.xDOI Listing

Publication Analysis

Top Keywords

kcnq2 kcnq3
16
kcnq1-4 potassium
8
potassium channels
8
channels expressed
8
expressed mammalian
8
muscarinic acetylcholine
8
acetylcholine receptors
8
kcnq3 channels
8
inhibition kcnq1-4
4
channels
4

Similar Publications

Article Synopsis
  • Variants associated with neurodevelopmental impairments in children are complex and challenging to evaluate due to their diverse nature and unclear causes.
  • The study highlights a case of a child with neonatal-onset epilepsy and a specific genetic variant (G256W) that impacts ion channel function and leads to reduced cell stability and conduction in nervous tissue.
  • The research also establishes a mouse model that exhibits epilepsy and hyperexcitability in brain cells, linking the genetic variant to observable neurological behaviors and suggesting potential wider implications for understanding similar conditions in other patients.
View Article and Find Full Text PDF

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.

View Article and Find Full Text PDF

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 PDF

Voltage- and Ca-inducible PLC activity for analyzing PI(4,5)P sensitivity of ion channels in Xenopus oocytes.

Biochim 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.

View Article and Find Full Text PDF

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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!