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ERG Components of Negative Polarity from the Inner Retina and the Optic Nerve Response


Niemeyer, Günter (2005). ERG Components of Negative Polarity from the Inner Retina and the Optic Nerve Response. Documenta ophthalmologica. Advances in ophthalmology, 111(3):179-189.

Abstract

ERG components of negative polarity in the light-adapted and in the dark-adapted inner retina are reviewed from a clinical perspective and include consideration of experimental research. Field potentials are inherently complex including summating contributions from specialized neurons as well as from glial elements. This property applies to the PERG, PhNR and to the STR. Experimental research can contribute to identifying the sites/cells of origins i.e. by determining depth profiles and by pharmacological manipulation. Intraretinal microelectrode-studies and pharmacological dissection of light-evoked responses have elucidated the origin of field potentials from the retinal pigment epithelium to the retinal ganglion cells. Thresholds for dark-adapted response components have been compared. Attenuation of the STR by anesthesia was found in cats in vivo when compared to threshold intensities used in isolated eye preparations in vitro, suggestive of depression of inner retinal activity by anesthetics. Evidence has been presented for antidromically elicited retinal responses of negative polarity that resemble the STR and summate with the light-evoked retinal response. This observation supports the notion that negative field potentials and components as recorded in the vitreous and at the cornea receive contributions from retinal ganglion cells. The weight of this contribution appears to vary among species, at least concerning the STR. The ocular negative reponses from the inner retina are compared to cortical excitatory mechanisms generating negativity in the baseline of the EEG

Abstract

ERG components of negative polarity in the light-adapted and in the dark-adapted inner retina are reviewed from a clinical perspective and include consideration of experimental research. Field potentials are inherently complex including summating contributions from specialized neurons as well as from glial elements. This property applies to the PERG, PhNR and to the STR. Experimental research can contribute to identifying the sites/cells of origins i.e. by determining depth profiles and by pharmacological manipulation. Intraretinal microelectrode-studies and pharmacological dissection of light-evoked responses have elucidated the origin of field potentials from the retinal pigment epithelium to the retinal ganglion cells. Thresholds for dark-adapted response components have been compared. Attenuation of the STR by anesthesia was found in cats in vivo when compared to threshold intensities used in isolated eye preparations in vitro, suggestive of depression of inner retinal activity by anesthetics. Evidence has been presented for antidromically elicited retinal responses of negative polarity that resemble the STR and summate with the light-evoked retinal response. This observation supports the notion that negative field potentials and components as recorded in the vitreous and at the cornea receive contributions from retinal ganglion cells. The weight of this contribution appears to vary among species, at least concerning the STR. The ocular negative reponses from the inner retina are compared to cortical excitatory mechanisms generating negativity in the baseline of the EEG

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Health Sciences > Ophthalmology
Life Sciences > Sensory Systems
Health Sciences > Physiology (medical)
Language:English
Date:1 November 2005
Deposited On:23 Oct 2018 14:56
Last Modified:31 Jul 2020 02:33
Publisher:Springer
ISSN:0012-4486
OA Status:Green
Publisher DOI:https://doi.org/10.1007/s10633-005-5504-8
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicencespringer101007s1063300555048 (Library Catalogue)

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