Extracellular calcium influx through L-type calcium channels, intracellular calcium currents and extracellular signal-regulated kinase signaling are involved in the abscisic acid-induced precognitive and anti-anxiety effects

Abstract

Abscisic acid (ABA), a critical phytohormone, is also produced in animal tissues. It has been reported that ABA has pro-cognitive and anti-anxiety effects in rats. However, its detailed mechanism has not yet been clarified. Here, the possible roles of extracellular and intracellular calcium store and ERK signaling were evaluated in pro-cognitive and anti-anxiety effects of ABA. Morris water maze (MWM) and plus maze tests were used to evaluate the learning and memory and anxiety-like behavior, respectively, in rats. The inhibitors of L- (nifedipine) and T-type (amiloride) calcium channels and endoplasmic reticulum Ca2+-ATPase (thapsigargin) were centrally (i.c.v.) injected 15 min before ABA. Hippocampal and prefrontal lobe levels of phosphorylated extracellular signal-regulated Kinase (p-ERK) were assessed by immunoblotting. The data showed that ABA has promoting effect on rat’s performance in MWM task and induced anti-anxiety effect. In addition, nifedipine and thapsigargin significantly prevented while, amiloride had no effect on the mentioned effects of ABA. Furthermore, p-ERK levels were significantly increased in ABA-treated rats which were inhibited by nifedipine and thapsigargin pretreatment. It seems that the extracellular calcium influx through L-type calcium channels, intracellular calcium storage and ERK signaling are involved, at least in part, in the pro-cognitive and anti-anxiety effects of ABA.