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Suresh Viswanathan

Publications and source records attributed to Suresh Viswanathan.

5 recordsLinked to original sources
PubMed2006

Multifocal pattern electroretinogram: cellular origins and clinical implications.

PURPOSES: The purposes of this article are to gain insight into the cellular origins of the multifocal pattern electroretinogram (mPERG) and evaluate its potential for clinical use. METHODS: mPERGs were recorded from four anesthetized monkeys before and after pharmacologic blockade of light-driven activity of inner-retinal neurons and from 55 normal human subjects (19-91 years) and six patients with glaucoma (43-77 years of age). Stimuli consisted of counterphase-modulated black and white triangles organized in 61-scaled hexagons with mean luminance 100 cd/m2 and 100% contrast. The stimulus array subtended 31 degrees vertically and 37 degrees horizontally at 48 cm. The amplifier cutoff frequencies were 3 and 100 Hz. Responses were grouped as quadrants and the first slice of the second-order kernel was analyzed. RESULTS: The mPERG responses of monkeys and humans were similar. In the monkey responses, there was an early positive potential (P1) around 25 ms and a later positive potential (P2) found selectively in the nasal field quadrants around 31 ms. These responses were seen around 22 and 36 ms in the human responses. After blockade of inner-retinal activity in monkeys, P1 amplitude was greatly reduced at all retinal locations and P2 was eliminated. P1 and P2 amplitudes were significantly reduced in the glaucomatous eyes relative to amplitudes of age-matched controls. Reductions in the amplitudes of P1 and P2 could easily discriminate between glaucomatous visual field quadrants with and without behavioral sensitivity losses. However, these alterations are likely to reflect diffuse losses. CONCLUSIONS: mPERG responses contain prominent contributions from inner-retinal neurons that can be reduced in glaucomatous eyes. These findings raise the possibility that the mPERG could be potentially useful in the objective estimation of neural damage in glaucoma. However, further refinement of recording techniques will be required if the mPERG is to be used to detect focal damage.

Adult↗
PubMed2002

Visual field defects and neural losses from experimental glaucoma.

Glaucoma is a relatively common disease in which the death of retinal ganglion cells causes a progressive loss of sight, often leading to blindness. Typically, the degree of a patient's visual dysfunction is assessed by clinical perimetry, involving subjective measurements of light-sense thresholds across the visual field, but the relationship between visual and neural losses is inexact. Therefore, to better understand of the effects of glaucoma on the visual system, a series of investigations involving psychophysics, electrophysiology, anatomy, and histochemistry were conducted on experimental glaucoma in monkeys. The principal results of the studies showed that, (1) the depth of visual defects with standard clinical perimetry are predicted by a loss of probability summation among retinal detection mechanisms, (2) glaucomatous optic atrophy causes a non-selective reduction of metabolism of neurons in the afferent visual pathway, and (3) objective electrophysiological methods can be as sensitive as standard clinical perimetry in assessing the neural losses from glaucoma. These experimental findings from glaucoma in monkeys provide fundamental data that should be applicable to improving methods for assessing glaucomatous optic neuropathy in patients.

Animals↗
PubMed2002

Inner-retinal contributions to the photopic sinusoidal flicker electroretinogram of macaques. Macaque photopic sinusoidal flicker ERG.

The purpose of this study was to examine inner-retinal contributions to the photopic sinusoidal flicker ERG. ERGs were recorded from 5 anesthetized monkeys to sinusoidally modulated (100%, 0.5-120 Hz) red full field flicker at Lmean of 3.2 log phot td on a rod saturating blue background (3.7 log scot td; 3.0 log phot td) before and after intravitreal injections of tetrodotoxin (TTX) to block Na+-dependent spikes of retinal ganglion and amacrine cells, followed by N-methyl-D-aspartate (NMDLA) to suppress all activity of these cells. Recordings also were made after blocking bipolar (and horizontal) cell responses with L-2-amino-4-phosphonobutyric acid (APB) and 2-cis-piperidine-2,3-dicarboxylic acid (PDA) or 6-cyano-nitroquinoxaline-2,3-dione (CNQX). Control fundamental (F1) and second harmonic (F2) amplitudes were large and variable at temporal frequencies up to 2 Hz. At higher frequencies, Fl amplitude was minimal with a phase step at a frequency between 13 and 19 Hz and maximal at 27-33 Hz. F2 was minimal at 2-3 Hz and maximal at 6-8 Hz, again with a phase step near the minimum. TTX, or NMDLA, produced small changes in Fl that shifted the amplitude minimum to a lower and the maximum to a higher frequency. In contrast, F2 was more strongly affected; both the amplitude minimum (and phase step) and maximum were greatly attenuated, leaving a moderate response from 0.5 to 8 Hz, which then declined as frequency was increased to 30 HZ. After APB and PDA or CNQX, F1 decreased continuously with increasing frequency and F2 was generally much smaller. The nearly linear F1 phase plotwas consistent with the presence of a single mechanism (i.e. photoreceptors). Inner-retinal neurons contribute to the photopic sinusoidal flicker ERG. Whereas for F1, inner-retinal contributions are small relative to those from bipolar cells; for F2, they are equal or greater between 2and 16 Hz.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2002

Retinal origins of the primate multifocal ERG: implications for the human response.

PURPOSE: To better understand the cellular contributions to the human multifocal ERG (mfERG), rhesus monkey and human mfERGs were recorded using the same stimulus conditions. The monkey mfERGs were recorded before and after injections of pharmacologic agents known to selectively block activity of particular cells and circuits in the retina. METHODS: Photopic mfERGs were recorded with Dawson-Trick-Litzkow (DTL) fiber electrodes from 16 eyes of 10 anesthetized adult rhesus monkeys (Macaca mulatta) and from 4 normal humans. The display consisted of 103 equal-sized hexagons within 17 degrees of the fovea. Monkey mfERGs were obtained before and after inner retinal responses were suppressed with intravitreal injections of tetrodotoxin (TTX), TTX+N-methyl-D-aspartic acid (NMDA), TTX+NMDA with the gamma-aminobutyric acid (GABA(A&C)) antagonist picrotoxin (PTX), or the inhibitory amino acid GABA and after L-2 amino-4-phosphonobutyric acid (APB) to block signal transmission to ON-bipolar cells. Finally, a combination of APB and cis-2,3 piperidine dicarboxylic acid (PDA) was used to isolate the contributions from the cone photoreceptors. RESULTS: TTX, which blocks sodium-based action potentials, removes a large contribution from the monkey's mfERG, but it does not remove all inner retinal influences. After administration of TTX, the mfERG is further modified by the addition of NMDA. TTX+NMDA, TTX+NMDA+PTX, or GABA alone have similar effects, suggesting that, at the concentrations used, they are largely removing the inner retinal contributions. After removing the inner retinal influences, the monkey's mfERG is mainly composed of ON- and OFF-bipolar contributions, as revealed after APB and PDA were injected. The leading edge of the first negative potential (N1) is largely shaped by the initial hyperpolarization of the OFF-bipolar cells. The photoreceptors also contribute to the leading edge of N1, but this contribution is small, except in the central 6 degrees. The depolarization of the ON-bipolars and the recovery of the OFF-bipolars contribute to the leading edge of the major positive component (P1), with the recovery of the ON-bipolars being the dominant influence on the trailing edge. The waveform of the human mfERG most closely resembles the rhesus monkey's mfERG after administration of TTX. CONCLUSIONS: The monkey's mfERG is shaped by large contributions from ON- and OFF-bipolar cells, combined with both spiking and nonspiking inner retinal contributions, and a small contribution from the photoreceptors. In comparison, the human mfERG resembles the monkey's mfERG after reduction of inner retinal contributions. Based on the pharmacologic dissection of the monkey's mfERG, a model of the waveform of the human mfERG is proposed. This model suggests that the waveform can be understood as a combination of overlapping ON- and OFF-bipolar cell contributions combined with smaller contributions from inner retina and photoreceptors.

Action Potentials↗