作者: M.A. Cenci
DOI: 10.1016/B978-0-12-802206-1.00043-X
关键词: Glutamatergic 、 Biology 、 Postsynaptic potential 、 Striatum 、 Dopamine 、 Abnormal involuntary movement 、 Parkinson's disease 、 Endocrinology 、 Glutamate receptor 、 Dyskinesia 、 Neuroscience 、 Internal medicine
摘要: The dopamine (DA) precursor, 3,4-dihydroxyphenyl-L-alanine (L-DOPA), is the most effective treatment for Parkinson's disease (PD), but causes dyskinesias (abnormal involuntary movements) in vast majority of patients. There a wide consensus that L-DOPA-induced dyskinesia (LID) depends on both pre- and postsynaptic disturbances nigrostriatal DA transmission. Presynaptically, LID associated with abnormal release defective clearance, which converge to cause large swings brain levels concomitant medication. Postsynaptically, dysregulation intracellular signaling gene expression downstream D1 receptor. These phenomena are particularly well studied striatum thus main topic this chapter. In addition, chapter reviews studies have revealed associations between different types abnormalities glutamatergic GABAergic transmission within cortico-basal ganglia circuits. (Less)