Intraretinal analysis of the a-wave of the electroretinogram (ERG) in dark-adapted intact cat retina.
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.
Kang Derwent
J J
JJ
Department of Biomedical Engineering, Northwestern University, Evanston, IL 60208-3107, USA.
Linsenmeier
R A
RA
D000613:Aminobutyrates / Q000494:pharmacology; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D002415:Cats; D003623:Dark Adaptation / Q000502:physiology*; D004596:Electroretinography / Q000295:instrumentation; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D007736:Kynurenic Acid / Q000494:pharmacology; D008839:Microelectrodes; D010775:Photic Stimulation; D020419:Photoreceptor Cells, Vertebrate / Q000502:physiology; D010875:Pipecolic Acids / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D012160:Retina / Q000187:drug effects / Q000502:physiology*; D013237:Stereoisomerism; D014822:Vitreous Body / Q000187:drug effects / Q000502:physiology
D000613:Aminobutyrates; D001552:Benzazepines; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D010875:Pipecolic Acids; D026902:Potassium Channel Blockers; C087873:DK-AH 268; C029262:2,3-piperidinedicarboxylic acid; D007736:Kynurenic Acid; C012729:2-amino-4-phosphonobutyric acid; C043636:zatebradine