Forchetti C, Scarnati E, Pacitti C, Agnoli A
Neurosci Lett. 1980 Dec;20(3):363-7. doi: 10.1016/0304-3940(80)90175-5.
An injection of D-tubocurarine into the rat striatum produces a complex motor syndrome resembling in part that induced by picrotoxin. The destruction of the dopaminergic terminals by 6-hydroxydopamine does not prevent these effects of D-tubocurarine on motor activity. Hence neither dopamine release nor the presynaptic acetylcholine receptors are responsible for the D-tubocurarine-induced movements. On the other hand, lesion of the striatum by kainic acid abolishes the motor abnormalities due to D-tubocurarine but not those due to picrotoxin injection. Therefore, the effects of picrotoxin might be attributable to an action on GABA receptors still present in the kainic acid-treated striatum, whereas the effects of D-tubocurarine might be due to its action on striatal postsynaptic acetylcholine receptors.
向大鼠纹状体注射筒箭毒碱会产生一种复杂的运动综合征，部分类似于由印防己毒素诱发的综合征。用6-羟基多巴胺破坏多巴胺能终末并不能阻止筒箭毒碱对运动活动的这些影响。因此，多巴胺释放和突触前乙酰胆碱受体均与筒箭毒碱诱发的运动无关。另一方面，用 kainic 酸损伤纹状体可消除由筒箭毒碱引起的运动异常，但不能消除因注射印防己毒素引起的运动异常。因此，印防己毒素的作用可能归因于其对 kainic 酸处理过的纹状体中仍然存在的GABA受体的作用，而筒箭毒碱的作用可能是由于其对纹状体突触后乙酰胆碱受体的作用。
