Rod and cone contributions to the a-wave of the electroretinogram of the macaque
The electroretinogram (ERG) of anaesthetised dark-adapted macaque monkeys was recorded in response to ganzfeld stimulation and rod- and cone-driven receptoral and postreceptoral components were separated and modelled. The test stimuli were brief (< 4.1 ms) flashes. The cone-driven component was i...
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Published in | The Journal of physiology Vol. 547; no. 2; pp. 509 - 530 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
The Physiological Society
01.03.2003
Blackwell Publishing Ltd Blackwell Science Inc |
Subjects | |
Online Access | Get full text |
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Summary: | The electroretinogram (ERG) of anaesthetised dark-adapted macaque monkeys was recorded in response to ganzfeld stimulation
and rod- and cone-driven receptoral and postreceptoral components were separated and modelled. The test stimuli were brief
(< 4.1 ms) flashes. The cone-driven component was isolated by delivering the stimulus shortly after a rod-saturating background
had been extinguished. The rod-driven component was derived by subtracting the cone-driven component from the mixed rodâcone
ERG. The initial part of the leading edge of the rod-driven a -wave scaled linearly with stimulus energy when energy was sufficiently low and, for times less than about 12 ms after the
stimulus, it was well described by a linear model incorporating a distributed delay and three cascaded low-pass filter elements.
Addition of a simple static saturating non-linearity with a characteristic intermediate between a hyperbolic and an exponential
function was sufficient to extend application of the model to most of the leading edge of the saturated responses to high
energy stimuli. It was not necessary to assume involvement of any other non-linearity or that any significant low-pass filter
followed the non-linear stage of the model. A negative inner-retinal component contributed to the later part of the rod-driven
a -wave. After suppressing this component by blocking ionotropic glutamate receptors, the entire a -wave up to the time of the first zero-crossing scaled with stimulus energy and was well described by summing the response
of the rod model with that of a model describing the leading edge of the rod-bipolar cell response. The negative inner-retinal
component essentially cancelled the early part of the rod-bipolar cell component and, for stimuli of moderate energy, made
it appear that the photoreceptor current was the only significant component of the leading edge of the a -wave. The leading edge of the cone-driven a -wave included a slow phase that continued up to the peak, and was reduced in amplitude either by a rod-suppressing background
or by the glutamate analogue, cis -piperidine-2,3-dicarboxylic acid (PDA). Thus the slow phase represents a postreceptoral component present in addition to
a fast component of the a -wave generated by the cones themselves. At high stimulus energies, it appeared less than 5 ms after the stimulus. The leading
edge of the cone-driven a -wave was adequately modelled as the sum of the output of a cone photoreceptor model similar to that for rods and a postreceptoral
signal obtained by a single integration of the cone output. In addition, the output of the static non-linear stage in the
cone model was subject to a low-pass filter with a time constant of no more than 1 ms. In conclusion, postreceptoral components
must be taken into account when interpreting the leading edge of the rod- and cone-driven a -waves of the dark-adapted ERG. |
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Bibliography: | J. Ahmed: Rose‐Hulman Institute of Technology, Department of Applied Biology and Biomedical Engineering, 5500 Wabash Avenue, Terre Haute, IN 47803, USA. Author's present address ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author's present address J. Ahmed: Rose-Hulman Institute of Technology, Department of Applied Biology and Biomedical Engineering, 5500 Wabash Avenue, Terre Haute, IN 47803, USA. |
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2002.030304 |