| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 From the College of Optometry, University of Houston, Houston, Texas.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
METHODS. ERGs were recorded with DTL electrodes from 62 normal subjects (16 to 82 years), 18 POAG patients (47 to 83 years) and 7 POAG suspects (46 to 73 years) to brief flashes (<6 ms), and also in a few subjects to long (200 ms) red, full-field ganzfeld flashes delivered on a rod-saturating blue background. At the time of ERG measurements, the intraocular pressures of most of the patients were controlled medically. Visual field sensitivities were measured with the Humphrey C24-2 threshold test and optic nerve head cup-to-disc ratio (C/D) was determined by binocular indirect ophthalmoscopy.
RESULTS. ERGs of normal subjects contained a slow negative potential following the a- and b-waves, the PhNR, that increased slightly in latency with age. The a- and b-wave amplitudes and implicit times of POAG patients were similar to age-matched controls. In contrast, their PhNRs were small or virtually absent. PhNR amplitudes were reduced even when visual sensitivity losses were small, and were correlated significantly (P < 0.05) with mean deviation (MD), corrected pattern SD (CPSD), and C/D across the population of POAG patients whose MD losses ranged from 1 to 13 dB, CPSDs from 0 to 11 dB and C/Ds from 0.6 to 0.9. PhNRs of most POAG suspects also were small.
CONCLUSIONS. PhNR amplitudes in POAG patients are smaller than those of normal subjects. PhNR amplitudes are reduced when visual field sensitivity losses are mild and become even smaller as sensitivity losses increase. There is a potential role for the PhNR in early detection and possibly in monitoring the progression of glaucomatous damage.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Recent studies in monkeys and cats have shown that the slow negative potential, the photopic negative response (PhNR), that follows the b-wave (and if the flash duration is long appears again after the d-wave) originates from the inner retina. The PhNR probably arises as a consequence of spiking activity of retinal ganglion cells.7 8 9 It is substantially reduced in eyes of macaque monkeys with experimental glaucoma when visual field defects measured by behavioral perimetry are still mild.8 The results in macaques whose retinas are very similar to those of humans raise the possibility that the PhNR may be a sensitive measure of retinal dysfunction in patients with diseases that affect the inner retina. In the present study, we investigated whether the PhNR was reduced in the ERG of patients with primary open angle glaucoma (POAG). Similar to observations in macaques with experimental glaucoma we found that PhNRs were greatly reduced in the patients’ ERGs, whereas a- and b-waves were not significantly altered. These results indicate that the PhNR holds promise for the clinical evaluation of retinal function in POAG. Results from this study have appeared previously in abstract form.10 11
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
21 mm Hg on at least two consecutive occasions.
Table 1
shows the highest pretreatment IOP recorded from these
patients. The optic nerve head cup-to-disc ratio (C/D) as determined by
binocular indirect ophthalmoscopy was 0.6. Finally, they had
reproducible visual field defects on the Humphrey 24-2 threshold test
that includes at least two contiguous points in the same hemifield on
the total deviation probability plot at the <2% level. These
inclusion criteria are a subset of the criteria used in the
Collaborative Initial Glaucoma Treatment Study.12
At the
time of ERG recordings, the IOPs of all but 5 POAG patients were
controlled with glaucoma medication: patients 3 and 10 had discontinued
their medication and patients 4, 15, and 18 were never treated (see
Table 1
). Patients with ocular disease other than POAG were excluded
from the study. We also recorded ERGs from 7 other patients (patients19
through 25 in Table 1
), all of whom had a history of elevated IOP but
satisfied only one or the other of the remaining two inclusion
criteria. We classified these 7 patients as POAG suspects.
|
ERG Recordings and Signal Processing
ERGs were recorded differentially between DTL fiber
electrodes13
moistened with carboxymethylcellulose sodium
1% lying in the lower cul-de-sac of each eye. Each DTL fiber was
anchored with a dab of petroleum jelly near the inner canthus and
electrically connected by a clip lead at the outer canthus. An adhesive
silver/silver chloride EKG electrode (Sentry Medical Products, Irvine,
CA), placed on the forehead served as the ground. Pupils were fully
dilated (8 to 9 mm in diameter) with tropicamide (1%) and
phenylephrine hydrochloride (2.5%). Signals were amplified, filtered
(DC-300 Hz with a Tektronix model 5A22N amplifier), and digitized at 1
kHz with a resolution of 0.1 µV. To minimize drift associated with DC
recordings, the amplifier was reset to zero before each stimulus
presentation. Responses were averaged over 60 to100 stimulus
presentations. The largest Fourier component close to 60 Hz was removed
digitally. Repeated three-point weighted smoothing (0.25, 0.5, 0.25)
was sometimes used to eliminate noise at frequencies > 250 Hz.
Visual Stimulation
Full-field stimulation was produced with a ganzfeld by rear
illumination of a concave white diffuser (35 mm in diameter),
positioned very close to one eye. Subjects maintained fixation with the
nontested eye. Stimuli were red flashes of brief duration (<6 ms). In
a few subjects, long duration (200 ms) stimuli also were used. Flashes
were produced by light emitting diodes (LEDs; peak output, 630 nm;
half-height bandwidth, 40 nm) enclosed in a metal tube with matte white
surface, 50 mm from the ganzfeld surface. Flash strength was altered by
varying the LED pulse duration between 0.128 and 5.12 ms. Interstimulus
intervals were of adequate duration to avoid adaptive effects. Steady
background illumination sufficient to saturate the rods was provided by
blue LEDs (peak output, 450 nm; half-height bandwidth, 40 nm) driven by
a current source controlled by a digital-to-analog converter. Scotopic
luminances (cd/m2) were calibrated using an International
Light photometer (model IL1700; Newburyport, MA) with CIE scotopic
correction filters. Photopic luminance was calibrated using a Minolta
spectroradiometer (model CS1000; Minolta Camera Co., Ltd., Osaka,
Japan). Scotopic trolands (scot td) for the blue background (3.7 log
scot td), photopic trolands (phot td) for the 200-millisecond red
stimuli, and photopic troland seconds (phot td · s) for the
brief flashes were calculated for a pupil diameter of 9 mm, without a
correction for the Stiles–Crawford effect. These stimuli were selected
because they were similar to those used in the study of macaque
photopic ERG and the effects of experimental glaucoma that motivated
the present one.8
The stimuli are particularly effective
in eliciting the PhNR; alternative stimulus conditions are addressed
later.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
|
We also were interested in determining if the PhNR changed systematically with age. Unlike a- and b-waves whose peaks were well defined, the PhNR had a relatively broad trough, making it difficult to determine its exact implicit time. To be more confident of the implicit time, we grouped the normal subjects in age bins (of 10 years) and averaged the ERGs of the subjects in each bin. In general, the PhNR of the group-averaged response had a more clearly defined peak than the individual responses. This is illustrated with an example in the inset to Figure 2 where the thick line represents the averaged response of the 51- to 60-year-old age group for the standard intensity flash and the thin line represents the individual response of a 51-year-old female.
|
ERG Responses in POAG
Figure 3
shows the ERG of a 63-year-old patient (No. 6 in Table 1 ) with POAG
(right) and an age-matched control subject (left). The visual fields of
the patient (not shown) indicated substantial defects at the time of
ERG measurement, the MD was -16.2 dB (P < 0.5%) and
CPSD was 11 dB (P < 0.5%). The patient’s C/Ds were
0.9, both in the vertical and horizontal meridians, indicating a severe
loss of ganglion cell axons. The age-matched control had normal visual
field sensitivity and a normal C/D (0.3). The PhNR was reduced
considerably in the patient compared to the control subject. A small
positive deflection that is normally present on the falling edge of the
b-wave at the higher intensities (1.1 log phot td · s and above)
emerged as a more prominent wave. In contrast to the PhNR, the a- and
b-waves from the glaucomatous eye were in the normal range. The
findings illustrated for this patient were typical of those for the
POAG patients.
|
|
|
Most of the patients were medically treated at the time of the ERG
recordings, raising a potential inadequacy in the untreated normal
control group. However, the POAG population contained 5 patients who
were not receiving medical treatment. The PhNR amplitudes for these
patients for whom the glaucoma variable was better isolated were well
distributed across the range for the other patients (see Table 1
).
Further, individual treated patients were using medications with
different mechanisms of action: ß-blocker (Timoptic, Betagan,
Betoptic), an 
-agonist (Alphagan) and a prostaglandin inhibitor
(Xalatan).
We compared the y-intercepts and slopes of the best-fitting
lines through the patient (thick lines) and age-matched control (thin
lines) data illustrated in Figures 4
and 5
. The difference in the
y-intercepts for the PhNR amplitudes approached significance
(P < 0.055), whereas all other differences were not
significant (P 0.3). Comparisons of the PhNR
implicit time of patients and age-matched control subjects were not
feasible because it was difficult to determine the implicit times of
reduced PhNRs. However, qualitatively, we did not discern obvious
differences in PhNR implicit times between individual patients and
their age-matched controls.
As shown in Figures 4 and 5 , there was substantial interindividual variation of PhNR and b-wave amplitudes in normal subjects. If the PhNR and b-wave amplitude varied similarly for each subject, then the ratio of the two amplitudes would show less variability and might prove to be a more useful measure than absolute PhNR amplitude. However, b-wave amplitudes were not significantly correlated with PhNR amplitudes, and the b-wave to PhNR ratios were actually less effective than PhNR amplitude in separating glaucomatous eyes from normal eyes (data not shown).
Sensitivity and Specificity of the PhNR in POAG
Receiver operating characteristic (ROC) curves were used to
evaluate the effectiveness of the PhNR amplitude in distinguishing
between normal and glaucomatous eyes.14
15
Figure 6
shows ROC curves for PhNR, a- wave and b-wave amplitudes. These curves
were generated by plotting sensitivity versus 1-specificity calculated
for different cutoff values (or criterion responses). Sensitivity shows
how well the PhNR amplitude performs as a test for detecting glaucoma.
High sensitivity indicates that the test has a low false-negative rate.
Specificity shows how well the PhNR amplitude identifies those subjects
who do not have the disease. High specificity indicates that the test
has a low false-positive rate. The cutoff values were selected in
decrements of 1 µV from the range of values pooled from all POAG
patients and control subjects to the standard 1.7 log phot td · s
flash. As can be seen in Figure 6
and Table 2
, the area under the
curves (AOC) was largest (0.96) for the PhNR (circles) and smallest
(0.56) for the b-wave (triangles). Correspondingly, PhNR and b-wave
amplitudes had the smallest and largest general error rates (GER),
which reflects the total percentage of false-positives and
false-negatives (see Table 2
). The optimal cutoff amplitude for the PhNR indicated by lowest GER,
was 13 µV. The sensitivity and specificity associated with this
cutoff amplitude were 83% and 90%, respectively, indicating that the
criterion amplitude of 13 µV can quite effectively distinguish
glaucomatous from normal eyes. These results show that of the three ERG
potentials studied, only the PhNR provides good discrimination between
normal subjects and POAG patients.
|
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
There are numerous reports of alterations in retinal ganglion cells and their axons in glaucomatous eyes or eyes with elevated IOP16 17 18 19 20 21 22 23 24 and more recently changes in glial cells have been described.25 26 27 28 When considering these reports in the context of animal studies investigating the retinal origins of the PhNR cited later, it seems likely that the reduction of PhNR in POAG patients is associated with the reduced or altered activity of both retinal ganglion and glial cells.
In macaques, in addition to the effects of experimental glaucoma, the PhNR also is reduced by intravitreal injections of tetrodotoxin (TTX).8 9 TTX is a voltage-gated Na+-channel blocker that eliminates spiking activity in amacrine (interplexiform) and retinal ganglion cells.29 30 31 More distal retinal neurons traditionally have not been thought to produce Na+-dependent spikes, and TTX is not known to have direct effects on their activity. Of the spiking neurons in the retina, only the ganglion cells (and their axons) are generally believed to be affected by experimental glaucoma19 20 21 22 23 24 (but see Ref. 32 ). This suggests that the PhNR arises from the spiking activity of retinal ganglion cells.
In related experiments in cats (which also have a TTX-sensitive PhNR), the PhNR, recorded intraretinally with microelectrodes, was found to be most prominent near and within the optic disc where retinal ganglion cell axons dominate the tissue.7 Further, intravitreal injection of Ba2+, an ion that blocks K+ channels in glia,33 34 and blocks glial-mediated responses in the ERG (e.g., Ref. 35 ) selectively eliminated the PhNR from the photopic ERG.7 Its removal by Ba2+ suggests that the PhNR is mediated by K+ buffer currents in glia that are activated by an increase in extracellular [K+] resulting from the spiking activity of retinal ganglion cell axons.
Stimulus and Recording Conditions for Eliciting the PhNR
An interesting issue is why the PhNR and its alterations in the
photopic ganzfeld flash ERG of POAG patients were not described
previously. Part of the reason may lie in the stimulus conditions that
were used. Whereas ERG studies often use broadband white test stimuli
on white backgrounds, we used red test flashes on a rod-saturating blue
background. We initially selected these conditions simply to ensure
photopic stimulation. However, in our macaque studies, we discovered
that the conditions elicited a prominent PhNR.8
This does
not mean that stimuli must be red flashes on a blue
background to produce PhNRs. In another study in macaques, 1.7 Hz
modulation of a diffuse white field on an RGB monitor (42° x 37°,
mean luminance of 45 cd/m2) was found to be
adequate, although not optimal for producing PhNRs.9
Further, in human subjects, Colotto et al.36
recently
described PhNRs in normal and glaucomatous eyes in response to 2-Hz
modulation (92% contrast) of a 12° x 12° field on a computer
monitor (mean luminance 78 cd/m2). Although PhNR
amplitudes for their normal subjects were quite small (approximately 2
µV on average) compared to our present finding of approximately 20
µV, PhNRs in patients with open angle glaucoma were reduced
significantly.36
Finally, North et al.37
recently reported that a PhNR that can be elicited with stimuli that
selectively produce S-cone driven responses is reduced significantly in
POAG patients. Our stimuli in the present study would have missed this
S-cone driven response.
Monochromatic full-field test stimuli may produce more obvious PhNRs than broadband stimuli because they provide less opportunity for inhibitory center-surround interactions in the responses of spectrally opponent retinal ganglion cells. This could enhance ganglion cell responses, and increase the PhNR. Further, when both background and flash are both spectrally broadband, more opportunity exists for light adaptation of the cone pathways that produce responses to the test flashes. If inner retinal signals are adapted by backgrounds weaker than those affecting outer retinal signals (e.g., Ref. 38 ), then signals originating from hyperpolarizing bipolar cells, photoreceptors, and perhaps horizontal cells rather than from ganglion cells would provide the dominant negative potentials in the ERG. Supporting this suggestion is the pharmacological evidence that distally generated negative potentials dominate in macaque photopic ERGs when full field white flashes on white backgrounds are used.6
The recording conditions in our study also might have facilitated detection of the PhNR. For instance, we did not filter low temporal frequencies as is commonplace in ERG recordings in humans; we made DC recordings that would not distort slower contributions to the ERG than the a- and b-waves. With regard to electrode placement, whereas it is quite common to make bipolar recordings of ERGs from one eye, we recorded differentially across the eyes. This recording configuration might be particularly good for PhNR recording. Consistent with this idea, in their study of the optic nerve head component in the multifocal ERG, Sutter and Bearse39 pointed out that placing a reference electrode on the nonstimulated eye provides a conducting pathway for the optic nerve head component.
PhNR Reduction and Visual Field Defects
We observed that PhNR amplitudes could be markedly reduced when
the patients’ overall field losses (relative to the normal reference
field, i.e., their MDs) were as small as -2 dB, and that the PhNR
amplitudes showed a low (though significant) correlation with visual
field indices (see Figs. 7A
and 7B
). One possible explanation for the
correlations not being higher could be that the ganzfeld ERG reflects
reduced ganglion cell function from a retinal area much larger than
that covered by perimetric testing. The stimuli for the two tests
differed in other properties, for example, wavelength, which also could
have contributed to the low correlation. It is also possible that the
reduced PhNR amplitude reflects in part, alterations that may not
directly impact visual sensitivity, for example, early glial
alterations.
We also observed a low but significant correlation between PhNR and vertical C/D in POAG patients. The increased C/D in these patients indicates a loss of ganglion cell axons, and it is possible that with a more objective measure of nerve fiber layer thickness we might have obtained a better correlation. Again, however, glial alterations may have been a factor.
Effect of Age on the PhNR
The changes that we observed in the a- and b-wave implicit times
and amplitudes in normal subjects corroborate previous reports of
age-related changes in the photopic flash ERG.40
41
The
pattern ERG (PERG), a response that is predominantly of inner-retinal
origin, also has been reported to be reduced in amplitude with age
(e.g., Ref. 42
). We found, in addition, that the
implicit time of the PhNR increases significantly with age and the
amplitude tends to decrease although the latter effect was not
statistically significant. Although these findings demonstrate the
importance of taking age into account when studying ERG changes in
disease processes, it should be noted that the age-related decrease in
PhNR amplitude is not so large to preclude studies of patients with
glaucoma who generally tend to be middle-aged or older.
Relation to the PERG
We have shown that reduction in PhNR amplitude is a sensitive
indicator of glaucoma. Of the ERG tests currently in use, the PERG and
particularly the slow negative potential that peaks approximately 95
milliseconds after each contrast reversal in the transient PERG (the
N95, e.g., Ref. 43
) has been
shown in numerous studies to be altered in glaucomatous eyes (for
reviews, see Refs. 44
and 45
) and to be
very sensitive for the detection of glaucoma.46
In
macaques, the N95 of the transient PERG, like the
PhNR of the uniform field ERG, can be removed either by experimental
glaucoma or by intravitreal injections of TTX,9
indicating
a common origin for the two responses. This commonality is supported by
the finding in macaques that averaging of the photopic ERG responses to
luminance increments and decrements of a uniform field reversed at a
low temporal frequency (e.g., 1.7 Hz) quite adequately simulates the
transient PERG to low spatial frequency stimuli. By virtue of canceling
the linear components of the diffuse field response, the averaging
isolates the nonlinear components, the largest of which was the
N95 of the PERG.9
Although some care must be taken when comparing the PhNR and the PERG, it is quite likely that the PhNR in the flash ERG will be as sensitive as the N95 of the PERG in detecting glaucomatous damage. Some advantages of the PhNR over the PERG are that it is less affected by opacities in the ocular media, it does not require refractive correction, and it is a larger response than the PERG. Altogether, these results indicate a potential role for the PhNR in early detection and possibly in monitoring the progression of glaucomatous damage.
|
Acknowledgements |
|---|
|
Footnotes |
|---|
Supported by Research Grant R01EY06671 (LJF) and Core Grant P30 EY07751 from the National Eye Institute, Bethesda, Maryland, and an Ezell fellowship (SV) from the American Optometric Foundation, Rockville, Maryland.
Submitted for publication June 27, 2000; revised September 19, 2000; accepted October 6, 2000.
Commercial relationships policy: N.
Corresponding author: Laura J. Frishman, College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX 77204-6052. lfrishman{at}uh.edu
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  M. Kondo, Y. Kurimoto, T. Sakai, T. Koyasu, K. Miyata, S. Ueno, and H. Terasaki Recording Focal Macular Photopic Negative Response (PhNR) from Monkeys Invest. Ophthalmol. Vis. Sci., August 1, 2008; 49(8): 3544 - 3550. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. K. Mojumder, D. M. Sherry, and L. J. Frishman Contribution of voltage-gated sodium channels to the b-wave of the mammalian flash electroretinogram J. Physiol., May 15, 2008; 586(10): 2551 - 2580. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Machida, Y. Gotoh, Y. Toba, A. Ohtaki, M. Kaneko, and D. Kurosaka Correlation between Photopic Negative Response and Retinal Nerve Fiber Layer Thickness and Optic Disc Topography in Glaucomatous Eyes Invest. Ophthalmol. Vis. Sci., May 1, 2008; 49(5): 2201 - 2207. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Machida, D. Raz-Prag, R. N. Fariss, P. A. Sieving, and R. A. Bush Photopic ERG Negative Response from Amacrine Cell Signaling in RCS Rat Retinal Degeneration Invest. Ophthalmol. Vis. Sci., January 1, 2008; 49(1): 442 - 452. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. V. Rangaswamy, S. Shirato, M. Kaneko, B. I. Digby, J. G. Robson, and L. J. Frishman Effects of Spectral Characteristics of Ganzfeld Stimuli on the Photopic Negative Response (PhNR) of the ERG Invest. Ophthalmol. Vis. Sci., October 1, 2007; 48(10): 4818 - 4828. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Miyata, M. Nakamura, M. Kondo, J. Lin, S. Ueno, Y. Miyake, and H. Terasaki Reduction of Oscillatory Potentials and Photopic Negative Response in Patients with Autosomal Dominant Optic Atrophy with OPA1 Mutations Invest. Ophthalmol. Vis. Sci., February 1, 2007; 48(2): 820 - 824. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Ueno, M. Kondo, C.-H. Piao, K. Ikenoya, Y. Miyake, and H. Terasaki Selective Amplitude Reduction of the PhNR after Macular Hole Surgery: Ganglion Cell Damage Related to ICG-Assisted ILM Peeling and Gas Tamponade. Invest. Ophthalmol. Vis. Sci., August 1, 2006; 47(8): 3545 - 3549. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. V. Rangaswamy, W. Zhou, R. S. Harwerth, and L. J. Frishman Effect of Experimental Glaucoma in Primates on Oscillatory Potentials of the Slow-Sequence mfERG Invest. Ophthalmol. Vis. Sci., February 1, 2006; 47(2): 753 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. R. Lalonde, B. C. Chauhan, and F. Tremblay Retinal ganglion cell activity from the multifocal electroretinogram in pig: optic nerve section, anaesthesia and intravitreal tetrodotoxin J. Physiol., January 15, 2006; 570(2): 325 - 338. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. V. Bui, B. Edmunds, G. A. Cioffi, and B. Fortune The Gradient of Retinal Functional Changes during Acute Intraocular Pressure Elevation Invest. Ophthalmol. Vis. Sci., January 1, 2005; 46(1): 202 - 213. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. V. Rangaswamy, L. J. Frishman, E. U. Dorotheo, J. S. Schiffman, H. M. Bahrani, and R. A. Tang Photopic ERGs in Patients with Optic Neuropathies: Comparison with Primate ERGs after Pharmacologic Blockade of Inner Retina Invest. Ophthalmol. Vis. Sci., October 1, 2004; 45(10): 3827 - 3837. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Gotoh, S. Machida, and Y. Tazawa Selective Loss of the Photopic Negative Response in Patients With Optic Nerve Atrophy Arch Ophthalmol, March 1, 2004; 122(3): 341 - 346. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. V. Bui and B. Fortune Ganglion cell contributions to the rat full-field electroretinogram J. Physiol., February 15, 2004; 555(1): 153 - 173. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Fortune, L. Wang, B. V. Bui, G. Cull, J. Dong, and G. A. Cioffi Local Ganglion Cell Contributions to the Macaque Electroretinogram Revealed by Experimental Nerve Fiber Layer Bundle Defect Invest. Ophthalmol. Vis. Sci., October 1, 2003; 44(10): 4567 - 4579. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. V. Rangaswamy, D. C. Hood, and L. J. Frishman Regional Variations in Local Contributions to the Primate Photopic Flash ERG: Revealed Using the Slow-Sequence mfERG Invest. Ophthalmol. Vis. Sci., July 1, 2003; 44(7): 3233 - 3247. [Abstract] [Full Text] [PDF]
|
|
| |||||||
