Lyeth B G, Jiang J Y, Gong Q Z, Hamm R J, Young H F
Department of Surgery, Medical College of Virginia/Virginia Commonwealth University, Richmond, USA.
Neuropeptides. 1995 Jul;29(1):11-9. doi: 10.1016/0143-4179(95)90051-9.
We examined the effects of an exogenous mu opioid agonist and antagonist on systemic physiology and neurological outcome following TBI in the rat. Experiment I: [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) (0.1 nMol or 0.3 nMol in 5 microliters) (n = 10) or artificial CSF (n = 10) was administered 5 min prior to fluid-percussion brain injury (2.1 atmospheres). Motor performance was assessed on days 1-5 after TBI. The mu receptor agonist, DAMGO significantly reduced both beam-walking latency and body weight loss after injury (p < 0.05). DAMGO-treated rats (n = 5) did not differ from CSF-treated rats (n = 5) on either systemic arterial blood pressure or heart rate responses to injury. Experiment II: Beta-funaltrexamine (beta-FNA) (20.0 nMol in 5.0 microliters) (n = 10) or artificial CSF (n = 10) was administered (icv) to rats 5 min prior to fluid-percussion brain injury (1.8 atmospheres). Motor performance was assessed on days 1-5 after TBI. The mu receptor antagonist, beta-FNA, significantly increased beam-walking latency after injury (p < 0.05). beta-FNA-treated rats (n = 5) did not differ from CSF-treated rats (n = 5) on either systemic arterial blood pressure or heart rate responses to injury. Experiment III: Neither beta-FNA nor DAMGO affected motor performance in uninjured rats. These results suggest that activation of mu opioid receptors by exogenous agonists may provide protection against deficits in motor performance produced by fluid percussion brain injury.
我们研究了外源性μ阿片受体激动剂和拮抗剂对大鼠创伤性脑损伤（TBI）后全身生理和神经学转归的影响。实验I：在液压冲击性脑损伤（2.1个大气压）前5分钟，给予[D-丙氨酸2，N-甲基苯丙氨酸4，甘氨酸5-醇]-脑啡肽（DAMGO）（5微升中含0.1纳摩尔或0.3纳摩尔）（n = 10）或人工脑脊液（n = 10）。在TBI后的第1至5天评估运动功能。μ受体激动剂DAMGO显著缩短了损伤后横梁行走潜伏期并减轻了体重下降（p < 0.05）。接受DAMGO治疗的大鼠（n = 5）与接受脑脊液治疗的大鼠（n = 5）在对损伤的全身动脉血压或心率反应方面没有差异。实验II：在液压冲击性脑损伤（1.8个大气压）前5分钟，向大鼠脑室内注射β-芬太尼（β-FNA）（5.0微升中含20.0纳摩尔）（n = 10）或人工脑脊液（n = 10）。在TBI后的第1至5天评估运动功能。μ受体拮抗剂β-FNA显著延长了损伤后横梁行走潜伏期（p < 0.05）。接受β-FNA治疗的大鼠（n = 5）与接受脑脊液治疗的大鼠（n = 5）在对损伤的全身动脉血压或心率反应方面没有差异。实验III：β-FNA和DAMGO均未影响未受伤大鼠的运动功能。这些结果表明，外源性激动剂激活μ阿片受体可能对液压冲击性脑损伤所致的运动功能缺陷具有保护作用。
