中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2011年
11期
1022-1025
,共4页
肖经纬%孟会林%段化伟%张志荣%王健%鱼涛%郑敏%李斌%郑玉新
肖經緯%孟會林%段化偉%張誌榮%王健%魚濤%鄭敏%李斌%鄭玉新
초경위%맹회림%단화위%장지영%왕건%어도%정민%리빈%정옥신
丙烯酰胺%突触%神经元可塑性%突触素I
丙烯酰胺%突觸%神經元可塑性%突觸素I
병희선알%돌촉%신경원가소성%돌촉소I
Acrylamide%Synapses%Neuronal plasticity%Synapsin I
目的 探讨丙烯酰胺(ACR)对大鼠神经元突触可塑性的影响及机制.方法 24只Wistar大鼠按随机数字表完全随机分为对照组(腹腔注射5g/kg生理盐水)和染毒组(腹腔注射30 mg/kg ACR),每组12只,雌雄各半;采用神经行为学方法评价神经损伤状态,组织病理学法检测心、肝、脾、肺、肾等的超微结构改变,电镜观察脊髓背角突触结构参数的变化,免疫组化法检测大鼠突触特异位点突触素I (Synapsin I)的变化.结果 与对照组(雄性:1.00±0.00;雌性:1.00±0.00)比较,染毒组大鼠的步态评分明显增加(雄性:2.50 +0.55,t=-7.24,P<0.01;雌性:3.17±0.41,t=- 12.19,P<0.01).两组大鼠心、肝、脾、肺、肾等脏器未见病理改变.与对照组[雄性:(0.41±0.09)μm;雌性:(0.40±0.06)μm]比较,染毒组大鼠的突触活性带长度缩短[雄性:(0.15±0.05)μm,t=6.59,P< 0.05;雌性:(0.14±0.07)μm,t=7.26,P< 0.05].对照组和染毒组Synapsin I的定位一致,均位于脊髓背角灰质.对照组Synapsin I呈强阳性反应,而染毒组阳性信号减弱.半定量结果显示,与对照组(雄性:195.40±12.30;雌性:195.19±6.71)比较,染毒组Synapsin I的含量降低(雄性:60.90±29.19,t=10.40,P<0.05;雌性:67.56±20.23,t=15.65,P<0.05).结论ACR神经损伤过程中,大鼠突触结构发生了可塑性改变,并与Synapsin I的表达可能关联.
目的 探討丙烯酰胺(ACR)對大鼠神經元突觸可塑性的影響及機製.方法 24隻Wistar大鼠按隨機數字錶完全隨機分為對照組(腹腔註射5g/kg生理鹽水)和染毒組(腹腔註射30 mg/kg ACR),每組12隻,雌雄各半;採用神經行為學方法評價神經損傷狀態,組織病理學法檢測心、肝、脾、肺、腎等的超微結構改變,電鏡觀察脊髓揹角突觸結構參數的變化,免疫組化法檢測大鼠突觸特異位點突觸素I (Synapsin I)的變化.結果 與對照組(雄性:1.00±0.00;雌性:1.00±0.00)比較,染毒組大鼠的步態評分明顯增加(雄性:2.50 +0.55,t=-7.24,P<0.01;雌性:3.17±0.41,t=- 12.19,P<0.01).兩組大鼠心、肝、脾、肺、腎等髒器未見病理改變.與對照組[雄性:(0.41±0.09)μm;雌性:(0.40±0.06)μm]比較,染毒組大鼠的突觸活性帶長度縮短[雄性:(0.15±0.05)μm,t=6.59,P< 0.05;雌性:(0.14±0.07)μm,t=7.26,P< 0.05].對照組和染毒組Synapsin I的定位一緻,均位于脊髓揹角灰質.對照組Synapsin I呈彊暘性反應,而染毒組暘性信號減弱.半定量結果顯示,與對照組(雄性:195.40±12.30;雌性:195.19±6.71)比較,染毒組Synapsin I的含量降低(雄性:60.90±29.19,t=10.40,P<0.05;雌性:67.56±20.23,t=15.65,P<0.05).結論ACR神經損傷過程中,大鼠突觸結構髮生瞭可塑性改變,併與Synapsin I的錶達可能關聯.
목적 탐토병희선알(ACR)대대서신경원돌촉가소성적영향급궤제.방법 24지Wistar대서안수궤수자표완전수궤분위대조조(복강주사5g/kg생리염수)화염독조(복강주사30 mg/kg ACR),매조12지,자웅각반;채용신경행위학방법평개신경손상상태,조직병이학법검측심、간、비、폐、신등적초미결구개변,전경관찰척수배각돌촉결구삼수적변화,면역조화법검측대서돌촉특이위점돌촉소I (Synapsin I)적변화.결과 여대조조(웅성:1.00±0.00;자성:1.00±0.00)비교,염독조대서적보태평분명현증가(웅성:2.50 +0.55,t=-7.24,P<0.01;자성:3.17±0.41,t=- 12.19,P<0.01).량조대서심、간、비、폐、신등장기미견병리개변.여대조조[웅성:(0.41±0.09)μm;자성:(0.40±0.06)μm]비교,염독조대서적돌촉활성대장도축단[웅성:(0.15±0.05)μm,t=6.59,P< 0.05;자성:(0.14±0.07)μm,t=7.26,P< 0.05].대조조화염독조Synapsin I적정위일치,균위우척수배각회질.대조조Synapsin I정강양성반응,이염독조양성신호감약.반정량결과현시,여대조조(웅성:195.40±12.30;자성:195.19±6.71)비교,염독조Synapsin I적함량강저(웅성:60.90±29.19,t=10.40,P<0.05;자성:67.56±20.23,t=15.65,P<0.05).결론ACR신경손상과정중,대서돌촉결구발생료가소성개변,병여Synapsin I적표체가능관련.
Objective To explore effects of acrylamide on synaptic plasticity of rat neuron and its mechanisms.Methods 24 Wistar rats were divided into control and test groups randomly,12 rats in each group.The ratio of male and female in each group was 1∶ 1.Acrylamide (30 mg/kg) was administered to rats by intraperitoneal injection in test group and normal saline(5 g/kg) was given to rats in control group.The neurobehavioral and pathologic changes of heart,liver,spleen,lung and kidney were observed.Changes of parameters in synapse were recorded by electron microscope.As an important target of synapse,change of Synapsin I was measured by immunohistochemical method.Results Compared with the control group ( male:1.00 ±O.00; female:1.00 ±0.00),the gait score was increased significantly in ACR treated group (male:2.50 ±0.55,t=-7.24,P<0.01; female:3.17 +0.41,t=- 12.19,P<0.01).No obvious pathological changes of heart,liver,spleen,lung and kidney were found in all rats.Compared with the control group(male:(0.41 ±0.09)μm; female:(0.40 ±0.06)μm),the length of active zone of synapse was decreased significantly in ACR treated group ( male:( 0.15 ± 0.05 ) μ m,t =6.59,P < 0.05 ; female:(0.14 +0.07) μm,t =7.26,P <0.05).The width and postsynaptic density of synapse in ACR treated group had no significant difference with control group.The location of Synapsin I of control group and ACR treated group was both in gray matter of spinal dorsal horn.Compared with the control group (male:195.40 ± 12.30; female:195.19 ± 6.71 ),the concentration of Synapsin I was decreased significantly in ACR treated group (male:60.90 ±29.19,t=10.40,P<0.05; female:67.56 ±20.23,t=15.65,P<0.05).Conclusion Neuronal synaptic plasticity was found in damage of nervous system induced by acrylamide in rats,which might be associated with the expression of Synapsin I.