丘脑底核电刺激对猴偏侧帕金森病纹状体神经递质的影响
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摘要
丘脑底核(subthalamic nucleus, STN)电刺激(deep brain stimulation, DBS)目前已成为治疗中晚期帕金森病(Parkinson's disease, PD)的一项安全有效的治疗方法。但是关于STN DBS的作用机制尚不清楚。本研究通过对猴偏侧PD模型STN的长期慢性高频电刺激,观察纹状体区细胞外液多巴胺及其代谢产物和氨基酸的变化。结果提示慢性STN高频电刺激可以增加猴偏侧PD模型刺激侧纹状体多巴胺(DA)、谷氨酸(Glu)、γ-氨基丁酸(GABA)和牛磺酸(Tau)的含量。
Deep brain stimulation of subthalamic nucleus (STN DBS) is a safe and effective treatment for patients with mid or late stage Parkinson' s disease (PD). But the mechanism of STN DBS remained to be answered. We observed changes of extracellular dopamine , glutmate, gamma-aminobutyric acid and taurine in the corpus striatum of MPTP-induced hemiparkinsonian monkeys after long term chronic high frequency stimulation of STN. The results indicated that senior monkey PD models can be produced successfully by endovascular method;After long term high frequency stimulation, the content of extracellular dopamine, glutmate, gamma-aminobutyric acid and taurine in the corpus striatum of stimulated side increased significantly. The study showed that the levels of extracellular dopamine , glutmate, amma-aminobutyric acid and taurine in the corpus striatum of hemiparkinsonism rhesus monkeys can be improved by chronic STN DBS, which may play a role in the mechanism of STN DBS.
Deep brain stimulation of subthalamic nucleus (STN DBS) is a safe and effective treatment for patients with mid or late stage Parkinson' s disease (PD). But the mechanism of STN DBS remained to be answered. We observed changes of extracellular dopamine , glutmate, gamma-aminobutyric acid and taurine in the corpus striatum of MPTP-induced hemiparkinsonian monkeys after long term chronic high frequency stimulation of STN. The results indicated that senior monkey PD models can be produced successfully by endovascular method;After long term high frequency stimulation, the content of extracellular dopamine, glutmate, gamma-aminobutyric acid and taurine in the corpus striatum of stimulated side increased significantly. The study showed that the levels of extracellular dopamine , glutmate, amma-aminobutyric acid and taurine in the corpus striatum of hemiparkinsonism rhesus monkeys can be improved by chronic STN DBS, which may play a role in the mechanism of STN DBS.
引文
1 Benhvenatre H. Microdialysis theory and application. Progress in Neurobiology. 1990;35:195-201.
2 Vingerhoets, FJG, Snow, BJ, retrud, JW, et al. Positron emission tomographic evidence for progression of human MPTP-induced dopaminergic lesions. Ann. Neurol. 1994. 36(5), 765-770.
3 Clarkc CE, Boycc S, Robterson RG, et al. Drug-induced dyskinesia in primates rendered hemiparkinsoniam by intracarotid administration of MPTP. J Ncurol Sci, 1989, 90(3):307-314.
4 张进禄,刘玉军,鲁强等。单侧颈内动脉注入MPTP建立偏侧帕金森病灵长类模型的研究。首都医科大学学报。1998;19(1):1-4。
5 Bankiewicz, KS, Oldfield, EH, Chiueh, CC, et al. Hemiparkinsonism in monkeys after unilateral internal carotid artery infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Life Sci. 1986:39(1):7-16.
6 Meissner W, Prunier C, Guilloteau D. et al. Time-course of nigrostriatal degeneration in a progressive MPTP-lesioned macaque model of Parkinson's disease. Mol Neurobiol. 2003;28(3):209-218.
7 Castagnoli N Jr, Petzer JP, Steyn S. et al. Monoamine oxidase B inhibition and neuroprotection: studies on selective adenosine A2A receptor antagonists. Neurology. 2003;61(11):S62-68.
8 Hill MP, Bezard E, McGuire SG. et al. Novel antiepileptic drug levetiracetam decreases dyskinesia elicited by L-dopa and ropinirole in the MPTP-lesioned marmoset. Mov Disord. 2003;18(11):1301-1305.
9 Burns RS, Chiueh CC, Markey SP, et al. A primate model of parkinsonism: selective destruction of dopaminergic neurons in the pars compacta of the substantia nigra by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Proc Natl Acad Sci U S A. 1983;80(14):4546-4550.
10 汤克俭,徐德隆,余慧贞等。自制MPTP制备恒河猴帕金森病模型评价。中国神经精神疾病杂志。1991:17(2),162-163.
11 Luqin M R, Montoro RJ, Guillen J. et al.recovery of chronic parkinsonian monkeys by autotransplants of carotid body cell aggregates into puten. Neron 1999,22(4):743-750
12 Elsworth, JD, Taylor, JR, Sladek Jr, JR, et al. Striatal dopaminergic correlates of stable parkinsonism and degree of recovery in old-world primates one year after MPTP treatment. Neuroscience 2000. 95(4), 399-408.
13 Wullner, U, Pakzaban, P, Brownell, A. et al. Dopamine terminal loss and onset of motor symptoms in MPTP-treated monkeys: a positron emission tomography study with 11C-CFT. Exp. Neurol. 1994. 126(2), 305-309.
14 Klivenyi P, Andreassen OA, Ferrante Pd, et al. Mice deficient in cellular glutathione peroxidase show increased vulnerability to maloeate, 3-nitropropionic acid, and 1-me thyl-4-phenyl-1, 2, 5, 6-tetrnhydropyridine. J Neurosci, 2000, 20(1): 1-7.
15 Andreassen OA. Fermnte Pd, Dedeoglu A, et al. Mice witll a partial deficiency of manganese supe roxide dismutase show increased vulnerability to the mitechondrial toxins malonate, 3-nitropropionic acid. andMPTP. Exp Neurol, 2001, 167(1): 189-195.
2 Vingerhoets, FJG, Snow, BJ, retrud, JW, et al. Positron emission tomographic evidence for progression of human MPTP-induced dopaminergic lesions. Ann. Neurol. 1994. 36(5), 765-770.
3 Clarkc CE, Boycc S, Robterson RG, et al. Drug-induced dyskinesia in primates rendered hemiparkinsoniam by intracarotid administration of MPTP. J Ncurol Sci, 1989, 90(3):307-314.
4 张进禄,刘玉军,鲁强等。单侧颈内动脉注入MPTP建立偏侧帕金森病灵长类模型的研究。首都医科大学学报。1998;19(1):1-4。
5 Bankiewicz, KS, Oldfield, EH, Chiueh, CC, et al. Hemiparkinsonism in monkeys after unilateral internal carotid artery infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Life Sci. 1986:39(1):7-16.
6 Meissner W, Prunier C, Guilloteau D. et al. Time-course of nigrostriatal degeneration in a progressive MPTP-lesioned macaque model of Parkinson's disease. Mol Neurobiol. 2003;28(3):209-218.
7 Castagnoli N Jr, Petzer JP, Steyn S. et al. Monoamine oxidase B inhibition and neuroprotection: studies on selective adenosine A2A receptor antagonists. Neurology. 2003;61(11):S62-68.
8 Hill MP, Bezard E, McGuire SG. et al. Novel antiepileptic drug levetiracetam decreases dyskinesia elicited by L-dopa and ropinirole in the MPTP-lesioned marmoset. Mov Disord. 2003;18(11):1301-1305.
9 Burns RS, Chiueh CC, Markey SP, et al. A primate model of parkinsonism: selective destruction of dopaminergic neurons in the pars compacta of the substantia nigra by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Proc Natl Acad Sci U S A. 1983;80(14):4546-4550.
10 汤克俭,徐德隆,余慧贞等。自制MPTP制备恒河猴帕金森病模型评价。中国神经精神疾病杂志。1991:17(2),162-163.
11 Luqin M R, Montoro RJ, Guillen J. et al.recovery of chronic parkinsonian monkeys by autotransplants of carotid body cell aggregates into puten. Neron 1999,22(4):743-750
12 Elsworth, JD, Taylor, JR, Sladek Jr, JR, et al. Striatal dopaminergic correlates of stable parkinsonism and degree of recovery in old-world primates one year after MPTP treatment. Neuroscience 2000. 95(4), 399-408.
13 Wullner, U, Pakzaban, P, Brownell, A. et al. Dopamine terminal loss and onset of motor symptoms in MPTP-treated monkeys: a positron emission tomography study with 11C-CFT. Exp. Neurol. 1994. 126(2), 305-309.
14 Klivenyi P, Andreassen OA, Ferrante Pd, et al. Mice deficient in cellular glutathione peroxidase show increased vulnerability to maloeate, 3-nitropropionic acid, and 1-me thyl-4-phenyl-1, 2, 5, 6-tetrnhydropyridine. J Neurosci, 2000, 20(1): 1-7.
15 Andreassen OA. Fermnte Pd, Dedeoglu A, et al. Mice witll a partial deficiency of manganese supe roxide dismutase show increased vulnerability to the mitechondrial toxins malonate, 3-nitropropionic acid. andMPTP. Exp Neurol, 2001, 167(1): 189-195.