Quinidine hydrochloride monohydrate

Cell experiment:

Mouse (m) Slo3 (KCa5.1) channels or mutant forms are expressed in Xenopus oocytes and currents recorded with 2-electrode voltage-clamp. Gain-of-function mSlo3 mutations are used to explore the state-dependence of the inhibition. The interaction between Quinidine hydrochloride monohydrate and mSlo3 channels is modelled by in silico docking[1].

Animal experiment:

24 rats are randomly divided into three groups with eight rats in each group. Groups Q1, Q3, and Q5 receive Quinidine hydrochloride monohydrate 1, 3, and 5 μmol, respectively, in 5 % glucose 0.1 mL. The sciatic nerve is exposed by making an incision from the left sciatic notch to the distal thigh. The subcutaneous tissue is bluntly dissected to expose the biceps femoris. The sciatic nerve is freed from its investing fascia. The procedure is then repeated on the right side. The somato-sensory evoked potential (SSEP) and compound muscle action potentials (CMAP) are recorded at baseline, immediately after Quinidine hydrochloride monohydrate treatment, then every 15 min thereafter for 1 h, then every 30 min thereafter for 3 h. The animals are allowed to recover and then kept separately for 2 weeks. After performing behavioral examinations, electrophysiological examinations are performed with the animals under intra-peritoneal anesthesia[2].

References:

[1]. Wrighton DC, et al. Mechanism of inhibition of mouse Slo3 (KCa 5.1) potassium channels by quinine, quinidine and barium. Br J Pharmacol. 2015 Sep;172(17):4355-63.
[2]. Cheng KI, et al. Application of quinidine on rat sciatic nerve decreases the amplitude and increases the latency of evoked responses. J Anesth. 2014 Aug;28(4):559-68.