Ameliorative effect of gastrodin on 3, 3′-iminodipropionitrile-induced memory impairment in rats. (6th May 2015)

• Record Type: Journal Article
• Authors: Wang, Xiaona; Tan, Yuan; Zhang, Feng
• Is Part Of: Neuroscience letters. Volume 594(2015)
• Page Start: 40
• Page End: 45
• Publication Date: 2015-05-06
• Subjects: Gastrodin -- 3, 3′-Iminodipropionitrile -- 5-HT -- Passive avoidance task -- Hippocampus; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.03.049
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: We examined the effect of gastrodin on memory impairment induced by IDPN. GAS attenuated IDPN-induced memory retention deficit in the PA test. GAS reversed IDPN-induced reduction of 5-HT and elevation of 5-HT turnover. GAS alleviated increase of SERT and decrease of 5-HT1AR expression induced by IDPN. GAS may provide a novel strategy for IDPN-induced cognitive impairment. Abstract: 3, 3′-Iminodipropionitrile (IDPN), one of the nitrile derivatives inducing neurotoxicity, causes the dyskinetic syndrome and cognitive impairment. Gastrodin is widely used to treat neurological disorders and showed to improve cognitive functions. The present study aimed to determine whether treatment with gastrodin can attenuate IDPN-induced impairment of memory consolidation in the passive avoidance (PA) task, and to explore the possible neural mechanisms. Our results showed that intragastric administration of gastrodin (200 mg/kg) reversed the IDPN-induced impairment of memory consolidation as indicated by the prolonged retention latency in the PA task. Furthermore, gastrodin reverted IDPN-induced reduction of serotonin (5-HT) and elevation of serotonin turnover ratio. Gastrodin treatment prevented the increase of serotonin transporter (SERT) and the decrease of serotonin 1A (5-HT1A) receptor expression in the hippocampus of IDPN-treated rats. These results suggest that long-term gastrodin treatment could represent a novel pharmacological strategy for IDPN-induced memory impairment, as well that its protective effect is mediated through normalization of the serotoninergic system.