Laboratory Animal and Comparative Medicine ›› 2017, Vol. 37 ›› Issue (1): 15-19.DOI: 10.3969/j.issn.1674-5817.2017.01.004

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Effect of Lateral Ventricle Injection of Ganglioside Sodium on Learning and Memory in Rats with Cerebral Palsy

YANG Feng-xiang, ZHANG Xiao-qiao, LUO Xiu-ling   

  1. Department of Nerve rehabilitation Center, Taihe Hospital, Shiyan 442000, China
  • Received:2016-08-26 Online:2017-02-25 Published:2017-02-25

Abstract: Objective To study the mechanism of Ganglioside (GM) lateral ventricle injection on learning and memory ability of rats with cerebral palsy, and to provide theoretical basis for clinical treatment of cerebral palsy. Methods Thirty-six SPF rats were randomly divided into blank control group, model group and GM group. The model group and GM group were randomly divided into the model group and the SD group. After modeling, 1 days and 10, 20, 30 days with the brain localization of rat instrument by rat intracerebroventricular injection of GM administered after modeling and administration after the water maze experiment instrument to explore, navigation, suspension and slope experiments comparing the ability of learning and memory of rats and exercise the ability to change space. And using the ELISA method for the determination of acetylcholine in hippocampus (Ach) and orbital venous blood acetylcholinesterase (AChE) activity. Determination of brain tissue and calmodulin dependent protein kinase II (CaMKII) and calmodulin (CaM). Results Compared with the model group, the rats in group GM after treatment, the time of finding the platform and slope experiment time was significantly shortened, suspension time, the first quadrant and the residence time in the voyage prolonged; positioning latency, swimming distance shortened, the Ach level was decreased, and AChE activity was increased. the brain tissue of liquid CaMK and CaM increased (P<0.05). Conclusion In rat cerebral palsy model, GM could inhibit the synthesis of CaMKII and CaM, reduce hydrolysis of neuronal calcium protein and calcium influx. By blocking the signaling pathway of CaMKII, GM treatment increases the activity of Ach, reduces brain damage caused by cerebral ischemia and hypoxia, thus promoting repair and regeneration of lesioned nerves and subsequently learning and memory.

Key words: Ganglioside sodium, Acetylcholine, Calmodulin dependent protein kinase II(CaMKII), Calmodulin(CaM), Space exploration experiment, Learning and memory

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