title: Retinal pathway origins of the pattern electroretinogram (PERG).
abstract: OBJECTIVE
  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 μM), 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 (N95 and P50) amplitudes in transient PERGs, and their counterparts, N2 and P1 in simulations, to half-amplitude. PDA eliminated N95 and N2, but increased P50 and P1 amplitudes, in that it enhanced b-waves. As previously reported, severe experimental glaucoma or TTX eliminated photopic negative responses, N95, and N2; glaucoma eliminated P50 and reduced P1 amplitude; TTX reduced P50 and hardly altered P1. 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 P1 in simulations.
  
  
  CONCLUSIONS
  Transient PERG receives nearly equal amplitude contributions from ON and OFF pathways. N95 reflects spiking activity of ganglion cells; P50 reflects nonspiking activity as well. Steady state PERG, in contrast, reflects mainly spike-related ON pathway activity.
authors.affiliation: University of Houston College of Optometry, Houston, Texas 77204-2020, USA.
authors.forename: Xunda
authors.initials: X
authors.lastname: Luo
authors.forename: Laura J
authors.initials: LJ
authors.lastname: Frishman
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D003198:Computer Simulation; D004195:Disease Models, Animal; D004596:Electroretinography / Q000187:drug effects / Q000379:methods*; D005901:Glaucoma / Q000473:pathology* / Q000503:physiopathology*; D058449:Intravitreal Injections; D008253:Macaca mulatta; D012160:Retina / Q000166:cytology* / Q000502:physiology; D012165:Retinal Ganglion Cells / Q000502:physiology; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D014795:Visual Pathways / Q000166:cytology* / Q000502:physiology
chemical_list: D026941:Sodium Channel Blockers; D013779:Tetrodotoxin