Horizontal Saccade Dynamics After Childhood Monocular Enucleation

2013 ◽  
Vol 54 (10) ◽  
pp. 6463 ◽  
Author(s):  
Esther G. González ◽  
Linda Lillakas ◽  
Alexander Lam ◽  
Brenda L. Gallie ◽  
Martin J. Steinbach
Keyword(s):  
Monocular Enucleation ◽  
Horizontal Saccade

Saccadic Gain Modification: Visual Error Drives Motor Adaptation

1998 ◽  
Vol 80 (5) ◽  
pp. 2405-2416 ◽  
Author(s):  
Josh Wallman ◽  
Albert F. Fuchs
Keyword(s):  
Target Location ◽  
Rhesus Macaques ◽  
Motor Adaptation ◽  
Saccadic Eye Movements ◽  
Target Distance ◽  
Error Signal ◽  
Gain Adaptation ◽  
Horizontal Saccade ◽  
Corrective Saccades ◽  
Visual Error

Wallman, Josh and Albert F. Fuchs. Saccadic gain modification: visual error drives motor adaptation. J. Neurophysiol. 80: 2405–2416, 1998. The brain maintains the accuracy of saccadic eye movements by adjusting saccadic amplitude relative to the target distance (i.e., saccade gain) on the basis of the performance of recent saccades. If an experimenter surreptitiously moves the target backward during each saccade, thereby causing the eyes to land beyond their targets, saccades undergo a gradual gain reduction. The error signal driving this conventional saccadic gain adaptation could be either visual (the postsaccadic distance of the target from the fovea) or motoric (the direction and size of the corrective saccade that brings the eye onto the back-stepped target). Similarly, the adaptation itself might be a motor adjustment (change in the size of saccade for a given perceived target distance) or a visual remapping (change in the perceived target distance). We studied these possibilities in experiments both with rhesus macaques and with humans. To test whether the error signal is motoric, we used a paradigm devised by Heiner Deubel. The Deubel paradigm differed from the conventional adaptation paradigm in that the backward step that occurred during the saccade was brief, and the target then returned to its original displaced location. This ploy replaced most of the usual backward corrective saccades with forward ones. Nevertheless, saccadic gain gradually decreased over hundreds of trials. Therefore, we conclude that the direction of saccadic gain adaptation is not determined by the direction of corrective saccades. To test whether gain adaptation is a manifestation of a static visual remapping, we decreased the gain of 10° horizontal saccades by conventional adaptation and then tested the gain to targets appearing at retinal locations unused during adaptation. To make the target appear in such “virgin territory,” we had it jump first vertically and then 10° horizontally; both jumps were completed and the target spot extinguished before saccades were made sequentially to the remembered target locations. Conventional adaptation decreased the gain of the second, horizontal saccade even though the target was in a nonadapted retinal location. In contrast, the horizontal component of oblique saccades made directly to the same virgin location showed much less gain decrease, suggesting that the adaptation is specific to saccade direction rather than to target location. Thus visual remapping cannot account for the entire reduction of saccadic gain. We conclude that saccadic gain adaptation involves an error signal that is primarily visual, not motor, but that the adaptation itself is primarily motor, not visual.

Opioid receptors in the accessory optic system of the rat: Effects of monocular enucleation

1990 ◽  
Vol 5 (5) ◽  
pp. 497-506 ◽  
Author(s):  
R.A. Giolli ◽  
R.H.I. Blanks ◽  
Y. Torigoe ◽  
R.J. Clarke ◽  
J.H. Fallon ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Opioid Receptors ◽  
Receptor Binding ◽  
Mu Opioid Receptor ◽  
Mu Opioid Receptors ◽  
Mu Opioid ◽  
Mu Receptor ◽  
Monocular Enucleation ◽  
Mu Receptors ◽  
Opioid Receptor Binding

AbstractThe presence and concentrations of each of the three subtypes of opioid receptors (mu, kappa, and delta) has been studied in the accessory optic nuclei (dorsal, lateral, and medial terminal nuclei and the interstitial nucleus of the superior fasciculus, posterior fibers: DTN, LTN, MTN, and inSFp) in normal young rats with radioligands directed towards each opioid receptor subtype. The changes in mu opioid receptors have also been investigated in monocularly enucleated rats in which one eye was removed and the rats sacrificed at postoperative day (PO) 2, 3, 5, 7, 14, and 30. As the MTN is the only accessory optic nucleus of the rat large enough for semiquantitative evaluation, the mu receptor population of the MTN has been subjected to optical microdensitometric analysis.All four of the accessory optic nuclei (AOS nuclei) are found to contain exceedingly high levels of mu opioid receptor binding with the selective radioligand [3H]-[D-Ala, MePhe4, Gly-ol5] (DAGO), low levels of kappa opioid receptor binding using the radioligand [3H]-[ethylketocyclazocine] (EKC) together with the competing agents [D-Pro4]-morphiceptin and [D-Ser2, Thr6]-Leu-enkephalin, and an absence of delta opioid receptor binding with the radioligand [3H]-[D-A1a2, D-Leu5]-enkephalin (DADLE) combined with the competing agent [D-Pro4]-morphiceptin. Monocular enucleation, as studied on the mu opioid receptor population with this experimental approach, results in virtually a complete loss of mu opioid receptors throughout all four of the contralaterally located AOS nuclei, including both dorsal and ventral subdivisions of the medial terminal nucleus (MTNd, v). Kappa and delta receptors are very few (kappa receptors) or are lacking (delta receptors) in the AOS nuclei, and for this reason, the effects of monocular enucleation on these two opioid receptor subtypes have not been investigated. Monocular enucleation also produces a significant lowering in mu receptor binding in other primary optic nuclei (the lateral geniculate nuclei, nucleus of the optic tract, and superficial layers of the superior colliculus) and in the pars principalis of the medial geniculate nucleus (description of changes in mu receptors in non-accessory optic primary optic nuclei will be considered elsewhere).Microdensitometric study of the MTNd, v shows that the decreased binding of mu receptors in this nucleus is barely detectable (about 6%) at PO2 and rises to 6–15% at PO3. At PO5 receptor loss reaches approximately 62%, whereas at PO7 it is about 81% complete. At PO14 and PO30, the mu receptor loss is nearly complete at around 93%. Mu receptor loss involves all of the AOS nuclei contralateral, but none ipsilateral, to ocular enucleation, an observation entirely consistent with the overwhelmingly crossed (about 97%) nature of the retinofugal projection to the rat accessory optic nuclei. These opioid receptors represent a prominent feature in the AOS and other primary optic nuclei of the rat. Their role in visuomotor control remains uncertain but probably involves the fine-tuning of information concerned with compensatory eye movements.

scholarly journals Recording Horizontal Saccade Performances Accurately in Neurological Patients Using Electro-oculogram

10.3791/56934 ◽  
2018 ◽  
Author(s):  
Yasuo Terao ◽  
Hideki Fukuda ◽  
Yusuke Sugiyama ◽  
Satomi Inomata-Terada ◽  
Shin-ichi Tokushige ◽  
...  
Keyword(s):  
Neurological Patients ◽  
Horizontal Saccade

Monocular enucleation reduces immunoreactivity to the calcium-binding protein calbindin 28 kD in the Rhesus monkey lateral geniculate nucleus

1992 ◽  
Vol 9 (5) ◽  
pp. 471-482 ◽  
Author(s):  
R. Ranney Mize ◽  
Qian Luo ◽  
Margarete Tigges
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Optical Density ◽  
Calcium Binding ◽  
Striate Cortex ◽  
Binding Protein ◽  
Visual Deprivation ◽  
Calcium Binding Protein ◽  
Monocular Enucleation ◽  
Lateral Geniculate ◽  
Antibody Labeling

AbstractThe calcium-binding proteins calbindin (CaBP) and parvalbumin (PV) are important in regulating intracellular calcium in brain cells. PV immunoreactivity is reduced by enucleation in the lateral geniculate nucleus (LGN) and by enucleation and visual deprivation in the striate cortex of adult monkeys. The effects of enucleation and visual deprivation on CaBP immunoreactivity in the LGN are not known. We therefore have studied cells and neuropil in the LGN that are labeled by antibodies to CaBP in normal and visually deprived Rhesus monkeys to determine if there is an effect on this calcium-binding protein. One group of monkeys had one eye removed 2 weeks to 4.3 years before sacrifice. A second group had one eye occluded with opaque lenses from infancy without enucleation. A final group had one eye occluded long-term followed by short-term enucleation 2 weeks before sacrifice.In normal monkeys, CaBP-immunoreactive neurons were found throughout the LGN. They were sparsely distributed within the six main laminae, and more densely distributed within layer S and the interlaminar zones (ILZ). The labeled ILZ neurons had a distinct morphology, with fusiform somata and elaborate dendritic trees that were confined primarily to the ILZ. Most CaBP-labeled neurons in the main layers had dendrites that radiated in all directions from the soma. ILZ and main layer cells labeled by CaBP thus probably represent two different cell types.Monocular enucleation with or without occlusion produced a significant reduction in antibody labeling in the deafferented laminae. Field measures revealed an average 11.5% reduction in optical density in each deafferented lamina compared to its adjacent, nondeprived layer. The differences in field optical density between deprived and nondeprived layers were statistically significant. CaBP neurons were still visible, but the optical density of antibody labeling in these cells also was reduced. Occlusion without enucleation had no effect. Thus, deafferentation, but not light deprivation, reduces concentrations of CaBP in monkey LGN. This effect is different than that seen in striate cortex of adult monkeys, where visual deprivation as well as enucleation alters CaBP immunoreactivity.

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