title: Contribution of N-methyl-DL-aspartic acid (NMDA)-sensitive neurons to generating oscillatory potentials in Royal College of Surgeons rats.
abstract: OBJECTIVE
  We investigated how the N-methyl-DL-aspartic acid (NMDA) receptor contributes to generating oscillatory potentials (OPs) of the electroretinogram (ERG) in the Royal College of Surgeons (RCS) rat.
  
  
  METHODS
  Scotopic ERGs were recorded from dystrophic and wild-type congenic (WT) RCS rats (n = 20 of each) at 25, 30, 35, and 40 days of age. The stimulus intensity was increased from -2.82 to 0.71 log cd-s/m(2) to obtain intensity-response function. NMDA was injected into the vitreous cavity of the right eyes. The left eyes were injected with saline as controls. The P3 obtained by a-wave fitting was digitally subtracted from the scotopic ERG to isolate the P2. For the OPs, the P2 was digitally filtered between 65 and 500 Hz. The amplitudes of OP1, OP2, OP3, and OP4 were then measured and summed and designated as ΣOPs. The implicit times of OP1, OP2, and OP3 were also measured. The frequency spectra of the OPs were analyzed using fast Fourier transform (FFT).
  
  
  RESULTS
  The maximum ERG a- and b-waves as well as ΣOPs amplitudes reduced with age in dystrophic rats. Compared with intravitreal saline injection, administration of NMDA decreased ΣOPs amplitudes from 30 days of age in dystrophic rats, while it did not attenuate ΣOPs amplitudes in WT rats. The implicit times of the OPs of the maximum ERG were prolonged by NMDA injections in WT and dystrophic rats. NMDA/saline ratios of ΣOPs amplitudes area under the FFT curves were significantly lower in dystrophic rats from 30 days of age than that in WT rats.
  
  
  CONCLUSIONS
  In the early stage of photoreceptor degeneration, intravitreal NMDA injection attenuated OPs amplitudes in dystrophic rats. This indicates that NMDA receptors play a significant role in generating OPs amplitudes with advancing photoreceptor degeneration.
authors.affiliation: Departments of Ophthalmology, Iwate Medical University School of Medicine, 19-1 Uchimaru, Morioka, Iwate, 020-8505, Japan.
authors.forename: Tomomi
authors.initials: T
authors.lastname: Harada
authors.forename: Shigeki
authors.initials: S
authors.lastname: Machida
authors.forename: Tomoharu
authors.initials: T
authors.lastname: Nishimura
authors.forename: Daijiro
authors.initials: D
authors.lastname: Kurosaka
mesh_terms: D000818:Animals; D003623:Dark Adaptation / Q000502:physiology; D004195:Disease Models, Animal; D004596:Electroretinography / Q000187:drug effects*; D058449:Intravitreal Injections; D016202:N-Methylaspartate / Q000031:analogs & derivatives* / Q000633:toxicity; D009991:Oscillometry; D010775:Photic Stimulation; D020419:Photoreceptor Cells, Vertebrate / Q000502:physiology*; D051381:Rats; D011922:Rats, Mutant Strains; D012162:Retinal Degeneration / Q000503:physiopathology*; D055351:Retinal Neurons / Q000502:physiology*
chemical_list: D016202:N-Methylaspartate; C083705:N-methyl-DL-aspartic acid