摘要
观察左旋多巴诱发异动症 (LID)大鼠模型基底节区谷氨酸脱羧酶 (GAD)和胆碱乙酰转移酶 (CAT)表达的变化 ,探讨LID发生过程中纹状体神经元的可塑性。间断性给帕金森病 (PD)大鼠腹腔注射左旋多巴 2 8d(每天 1次 )制备LID大鼠模型 ,应用免疫组织化学方法观察基底节区GAD和CAT的表达。结果发现模型复制成功后出现了与人类LID相似的对侧上肢、躯干和口面部异常不自主运动 (AIM)。与正常组比较尾壳核及苍白球区GAD明显增加 ,黑质网状部GAD明显减少。尾壳核区CAT明显减少。提示慢性间断性给PD大鼠左旋多巴能复制出LID大鼠模型 ,其纹状体区GABA能投射神经元及胆碱能中间神经元功能发生了改变 ,与LID的发生可能有关。
To observe the changes in expression of glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) in the basal ganglia and to explore neural plasticity in striatum in levodopa-induced dyskinesia (LID) rat model, Parkinsons disease (PD) rats were intermittently given 28-day treatment with levodopa once daily to prepare rat model of LID, and immunohistochemical study was performed to observe the expression of GAD and CAT in the basal ganglia. The results demonstrated that pulsatile treatment with levodopa induced contralateral forelimb, trunk and orofacial abnormal involuntary movement (AIM) in PD rats, similar to LID in PD patients. Compared to normal group, expression of GAD significantly increased in the caudate-putamen(CPU) and globus pallidus(GP), but decreased in the substantia nigra pars reticula (SNr), and expression of CAT reduced in the CPU in the DA-denevated striatum in LID group. It was concluded that LID model in rats could be established by intermittent treatment with levodopa to PD rats, and the changes of activities of striatal GABAergic projective neurons and cholinergic interneurons were resulted, which could be involved in occurrence of LID.
出处
《基础医学与临床》
CSCD
北大核心
2004年第6期619-622,共4页
Basic and Clinical Medicine
基金
国家自然科学基金 (30 30 0 114 )
