Relationship between learning and memory capacities and levodopa in rat models of Parkinson’s disease
10.3969/j.issn.2095-4344.2014.07.015
- VernacularTitle:帕金森病大鼠模型学习记忆能力与左旋多巴的关系
- Author:
Hongxia XING
;
Yan YUAN
;
Sheng LIU
;
Chuang YIN
;
Jinhong HAN
;
Huicong ZHOU
;
Zhou SU
;
Shuangxi GUO
;
Yumei WANG
- Publication Type:Journal Article
- Keywords:
levodopa;
Parkinson’s disease;
learning;
acetylcholine esterase;
homocysteine
- From:
Chinese Journal of Tissue Engineering Research
2014;(7):1069-1075
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Classical drug for Parkinson’s disease is levodopa, but long-term application of levodopa can induce complications such as dyskinesias.
OBJECTIVE:To observe the effects of levodopa on learning and memory capacities of Parkinson’s disease rats and to study its mechanisms.
METHODS:The rat models of Parkinson’s disease were established using 6-hydroxydopamine. The 228 model rats were randomly divided into control group and experimental group. Rats in the experimental group were intraperitoneal y injected with 10, 20 and 30 mg/(kg?d) levodopa for 28 consecutive days. At 1, 3, 5, 7, 14 and 28 days after intraperitoneal injection, we observed the rats’ learning and memory capacities and tested plasma concentration of homocysteine and folic acid. Acetylcholinesterase activities in the rat hippocampus were measured. Hippocampal neurofibril ary tangles were observed using Bielschowsky staining.
RESULTS AND CONCLUSION:Increased dose of levodopa and prolonged application time obviously decreased learning and memory capacities in rats (P<0.001), increased plasma homocysteine levels, reduced folic acid levels (P<0.001), diminished acetylcholine esterase activities in the rat hippocampus (P<0.001), and increased neurofibril ary tangles in the rat hippocampus (P=0.000). Results suggested that a large dose of levodopa could significantly decrease the learning and memory capacities, and disease acetylcholine esterase activities, and increase neurofibril ary tangles in hippocampus. Its mechanism possibly associated with the increased plasma concentration of homocysteine.
