Retinal Pathway Origins of the Pattern Electroretinogram (PERG)
Retinal Pathway Origins of the Pattern Electroretinogram (PERG)
复制标题
DOI：
10.1167/iovs.11-8376
复制
发表时间：
2011-11-01
影响因子：
4.4
通讯作者：
Frishman, Laura J.
中科院分区：
文献类型：
--
作者：
Luo, Xunda;Frishman, Laura J.
目的。采用药物解剖、均匀场闪烁和PERG模拟等方法确定猕猴视网膜模式电图（PERG）的视网膜通路起源。在玻璃体内注射L-AP4（非APB）（2-氨基-4-磷酸丁酸，1.6-2.0 mM）前后，记录瞬时（2 Hz， 4次逆转/s）和稳态（8.3 Hz， 16.6次逆转/s） PERGs和均匀场ERGs，以防止ON通路反应；PDA（顺式2,3-哌啶二羧酸，3.3-3.8 mM），阻断超极化二级和所有三级视网膜神经元的活性；TTX（河豚毒素，6 μ M），以阻断Na+依赖性穗。我们还记录了患有晚期单侧实验性青光眼的猕猴的PERGs，并通过对均匀场闪光的平均ON和OFF反应进行了模拟。对于2 hz的刺激，L-AP4将瞬态PERGs的负向和正向（N-95和P-50）振幅，以及模拟中的对应物N-2和P-1的振幅降低到一半。PDA消除了N-95和N-2，但增加了P-50和P-1振幅，因为它增强了b波。如前所述，严重的实验性青光眼或TTX消除了光性阴性反应、N-95和N-2；青光眼P-50消失，P-1振幅降低；TTX降低了P-50，几乎没有改变P-1。对于8.3 hz的刺激，L-AP4消除了稳态PERG，降低了模拟PERG的振幅，而PDA增强了这两种反应。TTX将PERG振幅降低到一半以下；模拟的减少较少。阻断所有受体后活性可消除瞬态和稳态PERGs，但在模拟中留下少量残留的P-1。瞬态PERG从ON和OFF通路接收几乎相等的振幅贡献。N-95反映神经节细胞的尖峰活动；P-50也反映了非尖峰活动。相比之下，稳态PERG主要反映与spike相关的ON通路活性。（Invest Ophthalmol Vis Sci. 2011;52:8571-8584） DOI: 10.1167/iovs.11-8376
PURPOSE. To determine retinal pathway origins of pattern electroretinogram (PERG) in macaque monkeys using pharmacologic dissections, uniform-field flashes, and PERG simulations.METHODS. Transient (2 Hz, 4 reversals/s) and steady state (8.3 Hz, 16.6 reversals/s) PERGs and uniform-field ERGs were recorded before and after intravitreal injections of L-AP4 (not APB) (2-amino-4-phosphonobutyric acid, 1.6-2.0 mM), to prevent ON pathway responses; PDA (cis-2,3-piperidinedicarboxylic acid, 3.3-3.8 mM), to block activity of hyperpolarizing second-and all third-order retinal neurons; and TTX (tetrodotoxin, 6 mu M), to block Na+-dependent spiking. PERGs were also recorded from macaques with advanced unilateral experimental glaucoma, and were simulated by averaging ON and OFF responses to uniform-field flashes.RESULTS. For 2-Hz stimulation, L-AP4 reduced both negative-and positive-going (N-95 and P-50) amplitudes in transient PERGs, and their counterparts, N-2 and P-1 in simulations, to half-amplitude. PDA eliminated N-95 and N-2, but increased P-50 and P-1 amplitudes, in that it enhanced b-waves. As previously reported, severe experimental glaucoma or TTX eliminated photopic negative responses, N-95, and N-2; glaucoma eliminated P-50 and reduced P-1 amplitude; TTX reduced P-50 and hardly altered P-1. For 8.3-Hz stimulation, L-AP4 eliminated the steady state PERG and reduced simulated PERG amplitude, whereas PDA enhanced both responses. TTX reduced PERG amplitude to less than half; simulations were less reduced. Blockade of all postreceptoral activity eliminated transient and steady state PERGs, but left small residual P-1 in simulations.CONCLUSIONS. Transient PERG receives nearly equal amplitude contributions from ON and OFF pathways. N-95 reflects spiking activity of ganglion cells; P-50 reflects nonspiking activity as well. Steady state PERG, in contrast, reflects mainly spike-related ON pathway activity. (Invest Ophthalmol Vis Sci. 2011;52:8571-8584) DOI: 10.1167/iovs.11-8376