Kang Derwent J J, Linsenmeier R A
Department of Biomedical Engineering, Northwestern University, Evanston, IL 60208-3107, USA.
Vis Neurosci. 2001 May-Jun;18(3):353-63. doi: 10.1017/s0952523801183021.
It has often been assumed that the recovery of the a-wave from its trough is caused by the intrusion of the b-wave. This study examined the recovery following the a-wave trough using intraretinal recordings in dark-adapted intact cat retina. Adult cats were anesthetized and paralyzed. The vitreal ERG was recorded between the vitreous humor and a reference electrode near the eye. Intraretinal recordings were made by referencing a microelectrode to the vitreal electrode. Bright flashes of diffuse white light were used to elicit a- and b-waves. Intravitreal injections of 2-amino-4-phosphonobutyrate (APB), cis 2,3-piperidine dicarboxylic acid (PDA), and kynurenic acid (KYN) were used to block the responses of bipolar and horizontal cells. Intravitreal injections of UL-FS 49 or DK-AH 269 were used to block Ih, a hyperpolarization-activated potassium current. Since the microelectrode was referenced to the vitreal electrode, recordings from the inner retina showed only the oscillatory potentials and b-waves. In the inner retina, the potential was flat until the b-wave became measurable, approximately 17 ms from the onset of the flash. The a-wave started to appear as the microelectrode reached the photoreceptors and its amplitude increased with depth until the microelectrode reached the choroid. The a-wave peaked at approximately 8 ms in response to flashes that saturated its amplitude and then began to recover well before any inner retinal responses were apparent. After injections of APB, PDA, and KYN, vitreal and intraretinal recordings showed only the a-wave, which consisted of an increase to peak at approximately 10 ms followed by a recovery to a plateau which was reached at approximately 25 ms. Blockers of Ih reduced the recovery, but did not eliminate it. The a-wave peaks and partially recovers before the b-wave intrudes. Both phases survive blockers of second-order neurons which implies that the photoreceptors generate both the rising and recovery phase of the a-wave. The recovery phase may be due to a current generated by the inner segment of photoreceptors.
人们常常认为,a波从波谷恢复是由b波的侵入引起的。本研究利用暗适应完整猫视网膜的视网膜内记录,研究了a波波谷后的恢复情况。成年猫被麻醉并麻痹。在玻璃体液和眼睛附近的参考电极之间记录玻璃体视网膜电图。通过将微电极参考到玻璃体电极来进行视网膜内记录。使用漫射白光的明亮闪光来诱发a波和b波。玻璃体内注射2-氨基-4-膦酰丁酸(APB)、顺式2,3-哌啶二羧酸(PDA)和犬尿氨酸(KYN)来阻断双极细胞和水平细胞的反应。玻璃体内注射UL-FS 49或DK-AH 269来阻断Ih,一种超极化激活的钾电流。由于微电极参考了玻璃体电极,来自视网膜内层的记录仅显示振荡电位和b波。在视网膜内层,在b波变得可测量之前,电位是平坦的,大约在闪光开始后17毫秒。当微电极到达光感受器时,a波开始出现,其振幅随着深度增加,直到微电极到达脉络膜。响应使a波振幅饱和的闪光,a波在大约8毫秒达到峰值,然后在任何视网膜内层反应明显之前就开始很好地恢复。注射APB、PDA和KYN后,玻璃体和视网膜内记录仅显示a波,a波包括在大约10毫秒增加到峰值,然后恢复到大约25毫秒达到的平台期。Ih阻断剂降低了恢复,但没有消除它。a波在b波侵入之前达到峰值并部分恢复。两个阶段在二阶神经元阻断剂作用下仍然存在,这意味着光感受器产生a波的上升和恢复阶段。恢复阶段可能是由于光感受器内段产生的电流。