Pharmacological properties of motion vision in goldfish measured with the optomotor response

Mora-Ferrer, Carlos; Hausselt, Susanne; Hoffmann, R.; Ebisch, Boris; Schick, S.; Wollenberg, Katharina; Schneider, C.O.; Teege, Patrick; Jürgens, Karin

doi:10.1016/j.brainres.2005.07.073

Cited by 13 publications

(9 citation statements)

References 47 publications

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“…The existence of cholinergic amacrine cells in the zebrafish retina has been shown by several groups (Yazulla and Studholme, 2001;Arenzana et al, 2005); their functional analogy to Starburst amacrine cells of the mammalian retina, however, has not been established. Studies in the goldfish retina revealed that blockage of the nicotinic acetylcholine receptors ablates motion depending vision (Mora-Ferrer et al, 2005), suggesting a role for nAChreceptor mediated cholinergic neurotransmission in motion perception. This hypothesis is consistent with our data, showing that the optokinetic response is abolished in noir mutants, suggesting that cholinergic amacrine cell function is impaired and subsequently these cells wither.…”

Section: Discussionmentioning

confidence: 99%

Distinct Retinal Deficits in a Zebrafish Pyruvate Dehydrogenase-Deficient Mutant

2010

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Mutations in ubiquitously expressed metabolic genes often lead to CNS-specific effects, presumably because of the high metabolic demands of neurons. However, mutations in omnipresent metabolic pathways can conceivably also result in cell type-specific effects because of cell-specific requirements for intermediate products. One such example is the zebrafish noir mutant, which we found to be mutated in the pdhb gene, coding for the E1 ␤ subunit of the pyruvate dehydrogenase complex. This vision mutant is described as blind and was isolated because of its vision defect-related darker appearance. A detailed morphological, behavioral, and physiological analysis of the phenotype revealed an unexpected specific effect on the retina. Surprisingly, the cholinergic amacrine cells of the inner retina are affected earlier than the photoreceptors. This might be attributable to the inability of these cells to maintain production of their neurotransmitter acetylcholine. This is reflected in an earlier loss of motion vision, followed only later by a general loss of light perception. Since both characteristics of the phenotype are attributable to a loss of acetyl-CoA production by pyruvate dehydrogenase, we used a ketogenic diet to bypass this metabolic block and could indeed partially rescue vision and prolong survival of the larvae. The noir mutant provides a case for a systemic disease with ocular manifestation with a surprising specific effect on the retina given the ubiquitous requirement for the mutated gene.

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Section: Discussionmentioning

confidence: 99%

Distinct Retinal Deficits in a Zebrafish Pyruvate Dehydrogenase-Deficient Mutant

2010

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“…Many studies combine the use of behavioral measures such as testing of the optomotor reflex to obtain visual acuity and contrast sensitivity data with physiological readouts such as electroretinography or structural assays such as OCT to obtain a more comprehensive overall assessment of retinal and neuronal health of a given subject. These methods have been employed in combination to assess visual differences amongst mouse strains (Puk et al, 2008), visual deficits in zebrafish models (Allwardt et al, 2001; Bahadori et al, 2006; Biehlmaier et al, 2007; Bilotta et al, 2002; Brockerhoff, 2006; Brockerhoff et al, 1995; Kainz et al, 2003; Le et al, 2012; Stujenske et al, 2011; Van Epps et al, 2001), therapeutic effects of compounds in goldfish (Mora-Ferrer et al, 2005), normal retinal function (Ho et al, 2012), therapies in visually impaired mice (Boye et al, 2010) and rats (McGill et al, 2007). The correlation of these parameters with morphological changes in the retina (McGill et al, 2012a; McGill et al, 2012b), was used to assess changes during retinal degeneration (Barabas et al, 2013; Cammas et al, 2010; Pang et al, 2011; Samardzija et al, 2014; Wright et al, 2013) and dysfunction (Hoelter et al, 2008; Lodha et al, 2010), eye blast trauma (Bricker-Anthony et al, 2014), visual deficits in diabetes mouse (Aung et al, 2013; Aung et al, 2014) and rat models, after transgenic modification of RGCs (Tomita et al, 2010) or bipolar cells (Lagali et al, 2008) or after transplanting photoreceptors in the retina to improve vision (Schmucker and Schaeffel, 2006; Thompson et al, 2014).…”

Section: Future Developmentsmentioning

confidence: 99%

Psychophysical testing in rodent models of glaucomatous optic neuropathy

Grillo

Koulen

2015

Experimental Eye Research

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Processing of visual information begins in the retina, with photoreceptors converting light stimuli into neural signals. Ultimately, signals are transmitted to the brain through signaling networks formed by interneurons, namely bipolar, horizontal and amacrine cells providing input to retinal ganglion cells (RGCs), which form the optic nerve with their axons. As part of the chronic nature of glaucomatous optic neuropathy, the increasing and irreversible damage and ultimately loss of neurons, RGCs in particular, occurs following progressive damage to the optic nerve head (ONH), eventually resulting in visual impairment and visual field loss. There are two behavioral assays that are typically used to assess visual deficits in glaucoma rodent models, the visual water task and the optokinetic drum. The visual water task can assess an animal’s ability to distinguish grating patterns that are associated with an escape from water. The optokinetic drum relies on the optomotor response, a reflex turning of the head and neck in the direction of the visual stimuli, which usually consists of rotating black and white gratings. This reflex is a physiological response critical for keeping the image stable on the retina. Driven initially by the neuronal input from direction-selective RGCs, this reflex is comprised of a number of critical sensory and motor elements. In the presence of repeatable and defined stimuli, this reflex is extremely well suited to analyze subtle changes in the circuitry and performance of retinal neurons. Increasing the cycles of these alternating gratings per degree, or gradually reducing the contrast of the visual stimuli, threshold levels can be determined at which the animal is no longer tracking the stimuli, and thereby visual function of the animal can be determined non-invasively. Integrating these assays into an array of outcome measures that determine multiple aspects of visual function is a central goal in vision research and can be realized, for example, by the combination of measuring optomotor reflex function with electroretinograms (ERGs) and optical coherence tomography (OCT) of the retina. These structure-function correlations in vivo are urgently needed to identify disease mechanisms as potential new targets for drug development. Such a combination of the experimental assessment of the optokinetic reflex (OKN) or optomotor reflex (OMR) with other measures of retinal structure and function is especially valuable for research on GON. The chronic progression of the disease is characterized by a gradual decrease in function accompanied by a concomitant increase in structural damage to the retina, therefore the assessment of subtle changes is key to determining the success of novel intervention strategies.

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“…In vision research, the OKR (sometimes called optokinetic nystagmus, or optomotor response) is used widely as a measure of visual function in studies of disease and development [7], [8], [53]–[57]. It has also been employed as an indicator of drug effects in retinal pharmacology [58]–[62].…”

Section: Discussionmentioning

confidence: 99%

Die Fledermaus: Regarding Optokinetic Contrast Sensitivity and Light-Adaptation, Chicks Are Mice with Wings

Shi

Stell

2013

PLoS ONE

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BackgroundThrough adaptation, animals can function visually under an extremely broad range of light intensities. Light adaptation starts in the retina, through shifts in photoreceptor sensitivity and kinetics plus modulation of visual processing in retinal circuits. Although considerable research has been conducted on retinal adaptation in nocturnal species with rod-dominated retinas, such as the mouse, little is known about how cone-dominated avian retinas adapt to changes in mean light intensity.Methodology/Principal FindingsWe used the optokinetic response to characterize contrast sensitivity (CS) in the chick retina as a function of spatial frequency and temporal frequency at different mean light intensities. We found that: 1) daytime, cone-driven CS was tuned to spatial frequency; 2) nighttime, presumably rod-driven CS was tuned to temporal frequency and spatial frequency; 3) daytime, presumably cone-driven CS at threshold intensity was invariant with temporal and spatial frequency; and 4) daytime photopic CS was invariant with clock time.Conclusion/SignificanceLight- and dark-adaptational changes in CS were investigated comprehensively for the first time in the cone-dominated retina of an avian, diurnal species. The chick retina, like the mouse retina, adapts by using a “day/night” or “cone/rod” switch in tuning preference during changes in lighting conditions. The chick optokinetic response is an attractive model for noninvasive, behavioral studies of adaptation in retinal circuitry in health and disease.

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Pharmacological properties of motion vision in goldfish measured with the optomotor response

Cited by 13 publications

References 47 publications

Distinct Retinal Deficits in a Zebrafish Pyruvate Dehydrogenase-Deficient Mutant

Distinct Retinal Deficits in a Zebrafish Pyruvate Dehydrogenase-Deficient Mutant

Psychophysical testing in rodent models of glaucomatous optic neuropathy

Die Fledermaus: Regarding Optokinetic Contrast Sensitivity and Light-Adaptation, Chicks Are Mice with Wings

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