Parecoxib, a selective blocker of cyclooxygenase-2, directly inhibits neuronal delayed-rectifier K+ current, M-type K+ current and Na+ current

High Efficacy by GAL-021: A Known Intravenous Peripheral Chemoreceptor Modulator that Suppresses BKCa-Channel Activity and Inhibits IK(M) or Ih

“…In the next set of experiments, we tested if GAL-021 could have any effects on another type of K + current, namely I K(M) , stated presently in these cells [25,43]. To enhance the degree of I K(M) , we bathed cells in high-K + solution and filled up the pipette by using K + -containing solution.…”

“…They are the principal molecular components of the voltage-gated M-type currents (I K(M) ), the magnitude of which can widely regulate neuronal excitability. Once activated, they are characterized by a slow activating and deactivating property [22][23][24][25]. KCNQ2 and KCNQ3 were noted to be mutated in patients with benign familial neonatal convulsions (BFNC).…”

Bisoprolol, Known to Be a Selective β1-Receptor Antagonist, Differentially but Directly Suppresses IK(M) and IK(erg) in Pituitary Cells and Hippocampal Neurons

“…The KCNQ2, KCNQ3, and KCNQ5 genes are known to encode the core subunits of K V 7.2, K V 7.3 and K V 7.5 channels, respectively. The increased activity of these K + channels can generate the M-type K + current ( I K(M) ) which is characterized by the activation in response to low threshold voltage and, once activated, displays a slowly activating and deactivating property [17,18,19,20]. Targeting I K(M) is growingly recognized as an adjunctive regimen for the treatment of many neurological disorders associated with neuronal hyper-excitability, such as cognitive dysfunction, neuropathic pain and epilepsy [21,22,23,24].…”

Effectiveness of nalbuphine, a κ‐opioid receptor agonist and μ‐opioid receptor antagonist, in the inhibition of INa, IK(M), and IK(erg) unlinked to interaction with opioid receptors

“…The cells were kept in monolayer cultures in plastic disks containing DMEM supplemented with 100 μM hypoxanthine, 1 μM aminopterin, 16 μM thymidine, and 5% FBS, in a humidified incubator equilibrated with 90% air/10% CO 2 at 37°C. To induce neuronal differentiation of NG108‐16 cells, culture medium was replaced with a solution containing 1 mM dibutyryl cyclic AMP, and cells were cultured for 1–7 days (Liu, Hsiao, Wang, Liu, & Wu, ).…”

“…They were grown as a monolayer culture in 50-ml plastic culture flasks in a humidified 5% CO 2 /95% air environment at 37 C. In a separate set of experiments, mHippoE-14 neurons were preincubated with naloxone (30 μM) for 6 hours at 37 C. Clonal strain NG108-15 cell line was from European Collection of Cell Cultures (ECACC-88112302; Wiltshire, UK). The cells were kept in monolayer cultures in plastic disks containing DMEM supplemented with 100 μM hypoxanthine, 1 μM aminopterin, 16 μM thymidine, and 5% FBS, in a humidified incubator equilibrated with 90% air/10% CO 2 at 37 C. To induce neuronal differentiation of NG108-16 cells, culture medium was replaced with a solution containing 1 mM dibutyryl cyclic AMP, and cells were cultured for 1-7 days (Liu, Hsiao, Wang, Liu, & Wu, 2019).…”