Gross J, Lun A, Berndt C
Institute of Pathological and Clinical Biochemistry, Medical School (Charité), Humboldt University, Berlin, Federal Republic of Germany.
J Neural Transm Gen Sect. 1993;93(2):109-21. doi: 10.1007/BF01245341.
A rat model of a mild, chronic, early postnatal hypoxia, characterized by long-term consequences in the behavioural outcome, was used to study long-term consequences in the dopaminergic system. Exposure of newborn rats to an early postnatal hypoxia (hypobaric hypoxia, 11 kPa pO2 in the inspiratory air, 2nd-10th day of life, 10 hours daily) brings about the following lasting neurochemical changes: an increased stimulated dopamine release rate from striatum slices by about 30%, an increased low affinity, high capacity dopamine uptake into striatum synaptosomes by about 100%. The critical period to produce an increased release rate of dopamine was estimated as day 2-6 postnatally. There are no long-term changes in the concentration of dopamine and its metabolites and in the tyrosine hydroxylase activity in consequences of this early postnatal hypoxia. Treatment of newborn animals with L-DOPA (10-50 micrograms/g body weight) previous to hypoxia normalizes the DA release rate.
一种轻度、慢性、出生后早期缺氧的大鼠模型，其特点是行为结果具有长期后果，被用于研究多巴胺能系统的长期后果。将新生大鼠暴露于出生后早期缺氧环境（低压缺氧，吸入空气中的pO2为11 kPa，出生后第2 - 10天，每天10小时）会导致以下持久的神经化学变化：纹状体切片中多巴胺刺激释放率增加约30%，纹状体突触体中低亲和力、高容量多巴胺摄取增加约100%。产生多巴胺释放率增加的关键时期估计为出生后第2 - 6天。这种出生后早期缺氧不会导致多巴胺及其代谢物浓度以及酪氨酸羟化酶活性的长期变化。在缺氧前用L - DOPA（10 - 50微克/克体重）治疗新生动物可使多巴胺释放率恢复正常。
