Effects of artemisinin on action potentials from C-type nodose ganglion neurons
Abstract
AIM: To investigate the effects of artemisinin (Art) on the action potentials (AP) recorded from identified C-type nodose neurons and study its anti-arrhythmic and anesthetic mechanisms.
METHODS:Neonatal and adult rats were selected for the preparation of isolated nodose ganglia neurons (NGN) and nodose ganglion-vagus slice preparation. Somatic AP were recorded from both isolated and slice NGN using whole-cell patch technique. Conduction velocity (CV) was measured using slice preparation. The effects of Art on AP were evaluated with the reference to ketamine.
RESULTS: Effects of Art on AP were that: (1) AP depolarizing profiles were inhibited without changing resting membrane potential (RMP). The peak of AP (AP(peak)) and upstroke velocity (UV(APD50) and UV(max)) decreased markedly (P<0.01). (2) The duration of AP at the point of half repolarization (APD(50)) was obviously prolonged (P<0.01). (3) Art also slowed down AP repolarization profiles (downstroke velocity, DV(APD50), and DV(max)) and the peak of after-hyperpolarization (AHP(peak)) was less negative. (4) Total inward and outward currents over the course of AP were significantly reduced in the presence of Art. (5) CV did not changed by Art. (6) The effects of Art on AP were concentration-dependent and resembled with those of ketamine except for CV.
CONCLUSION: Art inhibited both depolarization and repolarization of AP, suggesting that the effects of Art were probably, due to the blockade of Na+ and K+ ion channels.
Keywords:
METHODS:Neonatal and adult rats were selected for the preparation of isolated nodose ganglia neurons (NGN) and nodose ganglion-vagus slice preparation. Somatic AP were recorded from both isolated and slice NGN using whole-cell patch technique. Conduction velocity (CV) was measured using slice preparation. The effects of Art on AP were evaluated with the reference to ketamine.
RESULTS: Effects of Art on AP were that: (1) AP depolarizing profiles were inhibited without changing resting membrane potential (RMP). The peak of AP (AP(peak)) and upstroke velocity (UV(APD50) and UV(max)) decreased markedly (P<0.01). (2) The duration of AP at the point of half repolarization (APD(50)) was obviously prolonged (P<0.01). (3) Art also slowed down AP repolarization profiles (downstroke velocity, DV(APD50), and DV(max)) and the peak of after-hyperpolarization (AHP(peak)) was less negative. (4) Total inward and outward currents over the course of AP were significantly reduced in the presence of Art. (5) CV did not changed by Art. (6) The effects of Art on AP were concentration-dependent and resembled with those of ketamine except for CV.
CONCLUSION: Art inhibited both depolarization and repolarization of AP, suggesting that the effects of Art were probably, due to the blockade of Na+ and K+ ion channels.