Cortical modulation of striatal function
Cortical modulation of striatal function
复制标题
纹状体功能的皮质调节
DOI：
10.1016/0006-8993(82)90277-3
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发表时间：
1982
期刊：
影响因子：
2.9
通讯作者：
G. Bartholini
中科院分区：
文献类型：
--
作者：
B. Scatton;P. Worms;K. Lloyd;G. Bartholini
本实验观察了双侧皮质纹状体投射或选择性双侧额叶皮质消融对纹状体功能相关行为和生化参数的影响。其中两种损毁几乎完全阻断了氟哌啶醇的促生作用：术后3天即可观察到这种作用，并持续至少3个月，与纹状体谷氨酸摄取减少平行。纹状体中的多巴胺、二羟基苯乙酸、乙酰胆碱和P物质水平以及胆碱乙酰转移酶和谷氨酸脱氢☐酶活性在术后10天和21天均未受到影响。在黑质，抽吸额叶皮质10天后P物质水平无明显变化，但术后21天谷氨酸☐降解酶降低。皮质损毁仅部分阻止纹状体乙酰胆碱浓度的降低，而不影响氟哌啶醇引起的纹状体二羟基苯乙酸的升高。最后，损毁皮质纹状体通路不能影响阿朴吗啡引起的纹状体乙酰胆碱水平的升高、预先加载了[~3H]胆碱的纹状体脑片中钾(20 MM)诱发的[~3H]乙酰胆碱释放的减少以及纹状体二羟苯乙酸浓度的降低。这些发现表明，额叶皮质影响锥体外体功能的机制在行为学上是拮抗多巴胺介导的事件。生化数据表明，这一机制不涉及纹状体多巴胺能和胆碱能神经元活性的改变。这一机制可能利用：(1)皮质纹状体谷氨酸能神经元，如损伤后纹状体谷氨酸摄取减少所提示的；(2)GABA能途径，如黑质谷氨酸十☐解酶活性的降低以及GABA受体激动剂恢复氟哌啶醇所致的过敏症。
The effect of bilateral section of the corticostriatal projections or of selective bilateral ablation of the frontal cortex on behavioral and biochemical parameters related to striatal function were investigated in the rat.Either lesion almost completely prevented the cataleptogenic action of haloperidol: this effect was observed as soon as 3 days and lasted for at least 3 months after surgery, paralleling a reduction in striatal glutamate uptake. Also, such lesions enhanced the apomorphine-induced stereotyped behavior (as measured 21 days after surgery).In the striatum, dopamine, dihydroxyphenylacetic acid, acetylcholine and substance P levels as well as choline acetyltransferase and glutamic acid decar☐ylase activities were unaffected 10 or 21 days after either type of lesion. In the substantia nigra, substance P levels were unchanged 10 days following suction of the frontal cortex, but glutamic acid decar☐ylase was reduced at 21 days postsurgery.Cortical lesions only partially prevented the reduction in striatal acetylcholine concentrations and did not affect the increase in striatal dihydroxyphenylacetic acid caused by haloperidol. Finally, lesions of the corticostriatal pathways failed to affect the apomorphine-induced increase in striatal acetylcholine levels, reduction of the potassium (20 mM) evoked [3H]acetylcholine release in striatal slices preloaded with [3H]choline and decrease of striatal dihydroxyphenylacetic acid concentrations.These findings indicate that the frontal cortex influences extrapyramidal function by a mechanism which — in behavioral terms — is antagonistic to dopamine-mediated events. As indicated by the biochemical data, this mechanism does not involve changes in striatal dopaminergic and cholinergic neuron activity.This mechanism may utilize: (1) corticostriatal glutamatergic neurons as suggested by the reduction in striatal glutamate uptake following lesions; and (2) GABAergic pathways as suggested by the reduction of nigral glutamic acid decar☐ylase activity as well as by the finding that GABA receptor agonists reinstate haloperidol-induced catalepsy.