Loidl C F, Herrera-Marschitz M, Andersson K, You Z B, Goiny M, O'Connor W T, Silveira R, Rawal R, Bjelke B, Chen Y
Department of Physiology and Pharmacology, Huddinge Hospital, Karolinska Institute, Stockholm, Sweden.
Neurosci Lett. 1994 Jul 4;175(1-2):9-12. doi: 10.1016/0304-3940(94)91065-0.
Asphyxia was induced in pups delivered by caesarean section on pregnant Sprague-Dawley rats. Rats within the last day of gestation were anaesthetised and hysterectomized. The uterus horns including the foetuses were placed in a water bath for various periods of time. Following asphyxia the uterus horns were opened. The pups were removed, stimulated to breathe, left to recover and given to surrogate mothers. Control and asphyctic pups were obtained from each mother. Rats surviving asphyctic periods longer than 20 min at 37 degrees C showed chronic deficits in the release of neurotransmitters monitored with microdialysis in the basal ganglia. The main change observed in 6-month-old male rats that underwent severe perinatal asphyxia was a marked decrease in striatal dopamine release, monitored under basal and D-amphetamine stimulated conditions, as compared with control (normal- or caesarean-delivered) rats. Striatal glutamate and aspartate levels were also decreased following asphyxia. In the substantia nigra, the main effect of asphyxia was a decrease of both gamma-aminobutyric acid (GABA) and aspartate levels. Thus, this study provides evidence that perinatal asphyxia leads to chronic deficits in neurotransmission in the basal ganglia.
对怀孕的斯普拉格-道利大鼠剖腹产分娩的幼崽进行窒息诱导。在妊娠最后一天的大鼠进行麻醉并切除子宫。将包含胎儿的子宫角置于水浴中不同时间段。窒息后打开子宫角。取出幼崽,刺激其呼吸,使其恢复并交给代孕母鼠。从每只母鼠获得对照幼崽和窒息幼崽。在37摄氏度下经历窒息时间超过20分钟存活的大鼠,在基底神经节中用微透析监测神经递质释放出现慢性缺陷。与对照(正常或剖腹产分娩)大鼠相比,在经历严重围产期窒息的6个月大雄性大鼠中观察到的主要变化是,在基础和D-苯丙胺刺激条件下监测到纹状体多巴胺释放显著减少。窒息后纹状体谷氨酸和天冬氨酸水平也降低。在黑质中,窒息的主要影响是γ-氨基丁酸(GABA)和天冬氨酸水平均降低。因此,本研究提供了证据表明围产期窒息导致基底神经节神经传递出现慢性缺陷。