Ganglion cell contributions to the rat full-field electroretinogram

Ganglion cell contributions to the rat full-field electroretinogram
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DOI:
10.1113/jphysiol.2003.052738
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发表时间:
2004-02-15
影响因子:
5.5
通讯作者:
Fortune, B
Fortune, B
中科院分区:
医学1区
文献类型:
--
作者:
Bui, BV;Fortune, B

文献摘要

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本研究的目的是确定神经节细胞(GCs)对大鼠全视场视网膜电图(ERG)的贡献。为此,视神经横断(ONTx)后纵向评估ERG。另外的研究使用玻璃体内注射药理学活性物质。使用定制的氯化银电极同时记录麻醉的成年布朗-挪威大鼠(氯胺酮:噻嗪:乙酰丙嗪,55:5:1 mg kg(-1))的双眼ERG。在黑暗适应和光适应条件下(150 cd m(-2)),通过Ganzfeld进行短暂的白色氙气放电。分别于ONTx (n = 8)或sham (n = 8)手术后1、2、3、4和9周获得ERGs。ONTx降低了暗位阈值反应(pSTR和nSTR)的正、负分量。较亮闪光的暗位ERG反应,包括a波、b波和振荡电位(OPs),不受ONTx的影响。ONTx降低了光b波和OPs。TTX (6 μ m)降低了pSTR和nSTR,但没有降低暗斑a波、b波和OPs。TTX对光性ERG的影响显著,超过了ONTx。在ontx后9周使用TTX对STR几乎没有额外的影响。使用GABA (10 mm)或NMDA (0.8 mm)抑制视网膜内反应可显着降低nSTR。AMPA/KA离子型谷氨酸受体拮抗剂6-氰基-7-硝基喹啉-2,3(1H,4H)-二酮(CNQX, 0.2 mm)或顺式-2,3-哌啶二羧酸(PDA, 5 mm)也获得了类似的结果;然而,两者也都减少了近40%的暗b波。相比而言,NMDA受体拮抗剂D(-)-2-氨基-7-磷酸庚酸(D- ap7,0.2 mm)单独作用无效,但D- ap7和CNQX联合作用完全消除了STR。本研究结果表明:(1)大鼠的pSTR和nSTR成分直接依赖于完整的GC反应,且无分泌细胞对这些成分的贡献相对较小;(2)较亮闪光暗位ERG响应分量受gc影响较小;(3)大鼠光性ERG也反映气相色谱信号,可作为气相色谱功能的额外有用测试;(4) TTX对大鼠光性ERG有显著影响,这种影响不是由GC电流引起的,而是由无峰细胞或丛状细胞的电压门控钠电流引起的;(5) ONTx后残留少量阴性STR,这可能是由三级视网膜细胞(最有可能是无突细胞)的分级反应产生的。
The purpose of this study was to determine what contributions are made to the rat full-field electroretinogram (ERG) by ganglion cells (GCs). To that end, the ERG was assessed longitudinally following optic nerve transection (ONTx). Additional studies were conducted using intravitreal injections of pharmacologically active substances. The ERG was recorded simultaneously from both eyes of anaesthetized adult Brown-Norway rats (ketamine: xylazine: acepromazine,55:5: I mg kg(-1)) using custom silver chloride electrodes. Stimuli were brief, white xenon discharges delivered via a Ganzfeld under dark-adapted and light-adapted conditions (150 cd m(-2)). ERGs were obtained 1, 2, 3, 4 and 9 weeks after ONTx (n = 8) or sham (n = 8) operations. ONTx reduced both positive and negative components of the scotopic threshold response (pSTR and nSTR). Scotopic ERG responses to brighter flashes, including a-waves, b-waves and oscillatory potentials (OPs) were unaffected by ONTx. ONTx reduced the photopic b-wave and OPs. TTX (6 mum) reduced the pSTR and nSTR, but not the scotopic a-wave, b-wave or OPs. TTX had dramatic effects on the photopic ERG, surpassing the effects of ONTx. TTX application 9 weeks post-ONTx had little additional effect on the STR. Inhibition of inner retinal responses using GABA (10 mm) or NMDA (0.8 mm) reduced the nSTR substantially. Similar results were obtained with antagonists of AMPA/KA ionotropic glutamate receptors 6-cyano-7-nitroquinoxaline-2,3(1H,4H)-dione (CNQX, 0.2 mm) or cis-2,3-piperidinedicarboxylic acid (PDA, 5 mm); however, both also reduced the scotopic b-wave by similar to40 %. By contrast, the NMDA receptor antagonist D(-)-2-amino-7-phosphonoheptanoic acid (D-AP7,0.2 mm) had no effect alone, but the combination of D-AP7 and CNQX completely abolished the STR. The results of this study indicate that: (1) both pSTR and nSTR components in the rat depend directly upon intact GC responses, and that amacrine cell contributions to these components are relatively small; (2) scotopic ERG response components to brighter flashes receive little influence from GCs; (3) the rat photopic ERG also reflects GC signals and may serve as an additional useful test of GC function; (4) TTX had dramatic effects on the rat photopic ERG that were not attributable to GC currents, but rather to voltage-gated sodium currents in amacrine or interplexiform cells; (5) a small residual negative STR persisted after ONTx that was likely to be generated by graded responses of third-order retinal cells, most likely amacrine cells.