Huang Eagle Yi-Kung, Tsai Tung-Han, Kuo Tung-Tai, Tsai Jing-Jr, Tsui Pi-Fen, Chou Yu-Ching, Ma Hsin-I, Chiang Yung-Hsiao, Chen Yuan-Hao
Department of Pharmacology, National Defense Medical Center, No. 161, Sec. 6, Minquan E. Rd., Neihu Dist., Taipei City 114, Taiwan, ROC.
Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, 4F, No. 325, 2nd Sec., Cheng-Kung Road, Neihu District, Taipei City 114, Taiwan, ROC.
Behav Brain Res. 2014 Jul 1;267:156-72. doi: 10.1016/j.bbr.2014.03.033. Epub 2014 Mar 25.
To investigate the effects of traumatic brain injury (TBI) on the dopamine system in the brain at different distances from the impaction site, we compared the release, reuptake, metabolism, and release probability of dopamine on the sides of the brain ipsilateral and contralateral to the injury at different time points after varying severities of fluid percussion injuries.
Tonic (1-pulse evoked) and bursting (10-pulse evoked) dopamine release changes in the ipsilateral and contralateral sides of the striatum resulting from mild (2-Pa) and severe (6-Pa) levels of fluid percussion injury were analyzed at the acute (2h and 24h), subacute (1 and 2 weeks), and chronic stages (4, 6, and 8 weeks) after injury by using fast scan cyclic voltammetry to measure brain slices. The metabolic rate of striatal dopamine was surveyed using high-performance liquid chromatography. The microglia reaction was analyzed using immunohistochemistry at each stage.
In 6-Pa injured animals, for both tonic and bursting dopamine release, reuptake and release probability were suppressed on both the ipsilateral and contralateral sides of the striatum from the acute to the chronic stage. These neuronal activities were also affected at the subacute stage on both sides of the striatum in 2-Pa injured animals. The turnover rate of dopamine was not affected in the 2-Pa injured animals but increased gradually during the chronic stage in the 6-Pa injured group.
TBI suppresses dopamine release and reuptake and affects the metabolic rate and release probability of dopamine on the sides of the nigrostriatal system both ipsilateral and contralateral to the injury during both the acute and subacute stages after the injury.
为了研究创伤性脑损伤(TBI)对脑内不同距离撞击部位的多巴胺系统的影响,我们比较了在不同严重程度的液压冲击伤后不同时间点,损伤同侧和对侧脑区多巴胺的释放、再摄取、代谢及释放概率。
采用快速扫描循环伏安法检测脑片,分析轻度(2帕斯卡)和重度(6帕斯卡)液压冲击伤后急性(2小时和24小时)、亚急性(1周和2周)及慢性期(4周、6周和8周)纹状体同侧和对侧的多巴胺紧张性(单脉冲诱发)和爆发性(10脉冲诱发)释放变化。使用高效液相色谱法测量纹状体多巴胺的代谢率。在每个阶段采用免疫组织化学分析小胶质细胞反应。
在6帕斯卡损伤的动物中,从急性到慢性期,纹状体同侧和对侧的多巴胺紧张性和爆发性释放、再摄取及释放概率均受到抑制。在2帕斯卡损伤的动物中,亚急性期纹状体两侧的这些神经元活动也受到影响。2帕斯卡损伤的动物中多巴胺周转率未受影响,但在6帕斯卡损伤组慢性期逐渐升高。
创伤性脑损伤在损伤后的急性和亚急性期均抑制多巴胺释放及再摄取,并影响损伤同侧和对侧黑质纹状体系统的多巴胺代谢率和释放概率。