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脑内黑质注入 kainic 酸:黑质非多巴胺能神经元以与多巴胺能神经元相反的方式控制姿势和行为的证据。

Intranigral kainic acid: evidence for nigral non-dopaminergic neurons controlling posture and behavior in a manner opposite to the dopaminergic ones.

作者信息

Olianas M C, De Montis G M, Concu A, Tagliamonte A, di Chiara G

出版信息

Eur J Pharmacol. 1978 Jun 1;49(3):223-32. doi: 10.1016/0014-2999(78)90097-3.

Abstract

The unilateral, intranigral administration of kainic acid (k.a.) produced a syndrome characterized by early sequelae of contra- and ipsilateral circling and by a chronic contralateral turning associated with moderate loss of neurons in the pars reticulata. The acute contralateral circling seems to be related to dopaminergic nigro-neostriatal neuron stimulation, since it was prevented by previous intranigral injections of 6-OHDA. The acute ipsilateral circling and the chronic contralateral turning, on the other hand, seem to be independent of the integrity of the dopaminergic system and may be due to an initial stimulation, followed by destruction, of a nigral neuronal system which mediates turning behavior in a manner opposite to that of nigro-striatal dopamine. Treatment with D-amphetamine or apomorphine changed the contralateral into ipsilateral turning, while haloperidol potentiated the contralateral turning. Bilateral injection of k.a. into the nigra resulted in chronic stereotyped sniffing and gnawing, which were not inhibited by haloperidol. Moreover, haloperidol did not produce catalepsy in these animals. It is suggested that the intranigral k.a. injection destroyed a neuronal system antagonistic to dopamine and resulted in a reduction of the response to DA-receptor stimulation of the c. striatum.

摘要

向黑质单侧注射 kainic 酸(k.a.)会引发一种综合征,其特征为早期出现对侧和同侧转圈的后遗症,以及与黑质网状部神经元中度丧失相关的慢性对侧旋转。急性对侧旋转似乎与多巴胺能黑质 - 新纹状体神经元刺激有关,因为事先向黑质内注射 6 - OHDA 可预防这种旋转。另一方面,急性同侧旋转和慢性对侧旋转似乎与多巴胺能系统的完整性无关,可能是由于一个黑质神经元系统最初受到刺激,随后被破坏,该系统以与黑质 - 纹状体多巴胺相反的方式介导旋转行为。用 D - 苯丙胺或阿扑吗啡治疗可使对侧旋转变为同侧旋转,而氟哌啶醇则增强对侧旋转。向黑质双侧注射 k.a. 会导致慢性刻板的嗅咬行为,氟哌啶醇对此无抑制作用。此外,氟哌啶醇在这些动物中不会产生僵住症。有人提出,向黑质内注射 k.a. 会破坏一个与多巴胺拮抗的神经元系统,并导致尾状核对 DA 受体刺激的反应降低。

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