Drapeau P
Department of Physiology, University of Maryland School of Medicine, Baltimore 21201.
Neurosci Lett. 1988 Feb 29;85(2):233-8. doi: 10.1016/0304-3940(88)90357-6.
Rats were injected intrastriatally with kainic acid and the viability of dopaminergic terminals two days following the injection was determined by comparing voltage dependent calcium uptake and dopamine release in isolated nerve endings. Evoked dopamine release remained normal following the lesion, but the initial rate of potassium stimulated calcium entry decreased by approximately 1/3. These results suggest that the excitotoxic lesion caused by acute intrastriatal injection of kainic acid results in retention of functional dopaminergic terminals.
向大鼠脑内纹状体注射 kainic 酸,通过比较分离的神经末梢中电压依赖性钙摄取和多巴胺释放,测定注射两天后多巴胺能终末的活力。损伤后诱发的多巴胺释放仍保持正常,但钾刺激的钙内流初始速率降低了约 1/3。这些结果表明,急性脑内纹状体注射 kainic 酸引起的兴奋性毒性损伤导致功能性多巴胺能终末得以保留。