Kryzhanovskiĭ G N, Makul'kin R F, Shandra A A, Godlevskiĭ L S, Rozhkov V S
Biull Eksp Biol Med. 1987 Jun;103(6):650-3.
The experiments on rats have shown that bilateral administration of kainic acid (0.1-0.15 microgram) into the rostral parts of caudate nuclei led to the development of hypokinesia and rigidity. An increase in the electrical activity--the formation of the generator of pathologically increased excitement (GPIE) was noted in a zone of kainic acid injection. Rigidity and hypokinesia were attenuated and the GPIE activity was depressed after cyclodol (1-10 mg/kg) or L-DOPA (100-200 mg/kg) administration. Combined administration of cyclodol (2 mg/kg) and L-DOPA (50 mg/kg) induced potentiated antiparkinsonian effect. Dopamine microinjections into the GPIE area depressed its activity and abolished rigidity and hypokinesia. These data suggest that the Parkinson syndrome develops under the influence of GPIE induced by kainic acid administration into caudate nuclei.
对大鼠的实验表明，向尾状核头部双侧注射海藻酸（0.1 - 0.15微克）会导致运动减少和强直。在海藻酸注射区域观察到电活动增加——形成了病理性兴奋增强发生器（GPIE）。给予环苯扎林（1 - 10毫克/千克）或左旋多巴（100 - 200毫克/千克）后，强直和运动减少得到缓解，GPIE活动受到抑制。联合给予环苯扎林（2毫克/千克）和左旋多巴（50毫克/千克）可诱导增强的抗帕金森效应。向GPIE区域微量注射多巴胺可抑制其活动，并消除强直和运动减少。这些数据表明，帕金森综合征是在向尾状核注射海藻酸诱导的GPIE影响下发展而来的。
