Objective: To analyze the effect of Gastrodiae Rhizoma polysaccharide (GRPS) on neutral transmitter in the immature rats with cerebral palsy. Method: A total of 58 SD immature rats were used in the experiment

and except in the blank control ones

common carotid arteries of all the left 48 rats were ligatured and combined with hypoxia treatment to establish cerebral palsy models in immature rats. The successfully modeled rats were randomly divided into model group

cerebrolysin group (2.5 mL·kg-1)

GRPS low (150 mg·kg-1) and high dose (300 mg·kg-1) groups. After treatment for 21 days

Y maze and diving platform experiment were used to explore the memory ability of rats. The levels of nitric oxide (NO)

acetylcholine esterase (ACHE)

5-hydroxytryptamin (5-HT)

noradrenaline (NE) and γ-aminobutyric acid (GABA) in cerebral cortex and hippocampus were measured by using ELISA or chemical method. Real-time PCR and ELISA were used to detect the expression levels of endothelial nitric oxide synthase (eNOS) mRNA and protein in brain. HE staining was used to observe the hippocampus tissue structure. Result: As compared with normal blank group

the error number in behavior was significantly increased in model group rats; the step down latency was decreased; and also

the levels of 5-HT

NE and GABA in cerebral cortex and hippocampus of model group rats were significantly decreased

while the levels of ACHE and Glu were increased significantly (P<0.05

P<0.01). As compared with the model group

the levels of NO

NE

5-HT

and eNOS in cerebral cortex and hippocampus of GRPS low and high dose group rats were increased

while the level of ACHE was decreased (P<0.05

P<0.01); the levels of NO

NE

and expression of eNOS in hippocampus of GRPS high dose group were increased

while the levels of ACHE were decreased (P<0.05

P<0.01). The regular cell position was observed in hippocampus of GRPS low and high dose groups

without edema. Conclusion: GRPS could improve the memory of cerebral palsy immature rats

and the mechanism may be associated with increasing NO

ACHE

NE

5-HT and eNOS levels in cerebral cortex and hippocampus

and protection on hippocampus tissue structure of rats.