中华眼科杂志
中華眼科雜誌
중화안과잡지
Chinese Journal of Ophthalmology
2013年
6期
521-525
,共5页
戴旭锋%庞继景%韩娟娟%戚艳
戴旭鋒%龐繼景%韓娟娟%慼豔
대욱봉%방계경%한연연%척염
视网膜%钙通()%视网膜电描记术%小鼠
視網膜%鈣通()%視網膜電描記術%小鼠
시망막%개통()%시망막전묘기술%소서
Retina%Calcium channels%Electroretinography%Mice
目的 探讨电压依赖性钙通道(VDCC)α1F亚单位在小鼠视网膜组织中的分布和意义.方法 实验研究.将70只小鼠分为两组,实验组为VDCC α1F-/-小鼠(突变纯合子),对照组为α1F+/+小鼠(野生型),每组35只.免疫荧光法检测两组小鼠视网膜组织中α1F亚单位的表达情况;两组小鼠于生后3、6、9、14 d和3个月分别行视网膜石蜡切片观察显微结构;并记录两组小鼠闪光视网膜电图(ERG).两组小鼠ERG振幅的比较采用独立样本t检验.结果 (1)实验组小鼠视网膜组织中VDCC α1F亚单位呈阴性表达;对照组小鼠视网膜组织中VDCC α1F亚单位呈阳性表达,主要分布于视网膜外丛状层(OPL),内丛状层和神经节细胞层可见少量表达.(2)α1F-/-小鼠出生后视网膜组织中的OPL逐渐变窄,至3个月龄时几乎消失;而α1F+/+小鼠视网膜OPL厚度始终变化不大.(3)α1F-/-小鼠暗适应标准强度闪光ERG b波振幅[(163.8±26.7)μV]较α1F+/+小鼠[(408.4±54.5)μV]明显降低(t=-9.017,P=0.000),而α1F-/-小鼠a波振幅[(208.2 ±27.3) μV]与α1F+/+小鼠[(196.0 ±24.2)μV]的差异无统计学意义(t=0.748,P=0.476).结论 VDCCα1F亚单位缺陷主要影响小鼠视网膜OPL的结构和功能.
目的 探討電壓依賴性鈣通道(VDCC)α1F亞單位在小鼠視網膜組織中的分佈和意義.方法 實驗研究.將70隻小鼠分為兩組,實驗組為VDCC α1F-/-小鼠(突變純閤子),對照組為α1F+/+小鼠(野生型),每組35隻.免疫熒光法檢測兩組小鼠視網膜組織中α1F亞單位的錶達情況;兩組小鼠于生後3、6、9、14 d和3箇月分彆行視網膜石蠟切片觀察顯微結構;併記錄兩組小鼠閃光視網膜電圖(ERG).兩組小鼠ERG振幅的比較採用獨立樣本t檢驗.結果 (1)實驗組小鼠視網膜組織中VDCC α1F亞單位呈陰性錶達;對照組小鼠視網膜組織中VDCC α1F亞單位呈暘性錶達,主要分佈于視網膜外叢狀層(OPL),內叢狀層和神經節細胞層可見少量錶達.(2)α1F-/-小鼠齣生後視網膜組織中的OPL逐漸變窄,至3箇月齡時幾乎消失;而α1F+/+小鼠視網膜OPL厚度始終變化不大.(3)α1F-/-小鼠暗適應標準彊度閃光ERG b波振幅[(163.8±26.7)μV]較α1F+/+小鼠[(408.4±54.5)μV]明顯降低(t=-9.017,P=0.000),而α1F-/-小鼠a波振幅[(208.2 ±27.3) μV]與α1F+/+小鼠[(196.0 ±24.2)μV]的差異無統計學意義(t=0.748,P=0.476).結論 VDCCα1F亞單位缺陷主要影響小鼠視網膜OPL的結構和功能.
목적 탐토전압의뢰성개통도(VDCC)α1F아단위재소서시망막조직중적분포화의의.방법 실험연구.장70지소서분위량조,실험조위VDCC α1F-/-소서(돌변순합자),대조조위α1F+/+소서(야생형),매조35지.면역형광법검측량조소서시망막조직중α1F아단위적표체정황;량조소서우생후3、6、9、14 d화3개월분별행시망막석사절편관찰현미결구;병기록량조소서섬광시망막전도(ERG).량조소서ERG진폭적비교채용독립양본t검험.결과 (1)실험조소서시망막조직중VDCC α1F아단위정음성표체;대조조소서시망막조직중VDCC α1F아단위정양성표체,주요분포우시망막외총상층(OPL),내총상층화신경절세포층가견소량표체.(2)α1F-/-소서출생후시망막조직중적OPL축점변착,지3개월령시궤호소실;이α1F+/+소서시망막OPL후도시종변화불대.(3)α1F-/-소서암괄응표준강도섬광ERG b파진폭[(163.8±26.7)μV]교α1F+/+소서[(408.4±54.5)μV]명현강저(t=-9.017,P=0.000),이α1F-/-소서a파진폭[(208.2 ±27.3) μV]여α1F+/+소서[(196.0 ±24.2)μV]적차이무통계학의의(t=0.748,P=0.476).결론 VDCCα1F아단위결함주요영향소서시망막OPL적결구화공능.
Objective To investigate the distribution and biological roles of voltage-dependent calcium channel (VDCC) α1F subunit in murine retina.Methods Experimental study.α1 F-/-(homozygous mutant) mice (n =35) and α1 F +/+ (wild type) mice (n =35) were used in this study.Immunohistochemistry was performed to determine the expression of VDCC α1F subunit in the mouse retina.Retinae in α1 F-/-mice and age-matched control mice at 3,6,9,14-day and 3-month after birth were paraffin embedded,sectioned and HE stained,and full-field electroretinogram (ERG) were also recorded at these time points.Statistics were based on independent samples t-test.Results (1) α1 F subunit was absent in o1F-/-mice retina.But in α1F+/+ mice retina,α1F subunit was expressed most strongly in the outer plexiform layer (OPL),less in the inner plexiform layer (IPL) and ganglion cell layer (GCL).(2) OPL thickness in the subunit deficient mice gradually reduced after birth and lost at adult age.(3) In darkadapted E RGs,standard response showed that the b-wave amplitude of α1 F-/-mice [(163.8 ± 26.7) μV]significantly decreased compared with that of α1 F +/+ mice [(408.4 ± 54.5) μV] (t =-9.017,P =0.000),whereas the a-wave amplitude ofα1F-/-group [(208.2 ±27.3) μV] was similar to that of control group [(196.0 ±24.2) μV] (t =0.748,P =0.476).Conclusion This study demonstrates that the lack of VDCC α1 F subunit affect the structure and function in the OPL of the murine retina.