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Sökning: WFRF:(McLoon Linda K)

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1.
  • Fast, Elizabeth, et al. (författare)
  • Eye vergence is limited by adaptation
  • 2016
  • Ingår i: Investigative Ophthalmology and Visual Science. - 0146-0404 .- 1552-5783. ; 57:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose : What limits vergence abilities? Current models propose that vergence movements are controlled by a phasic component, which responds to image disparities, and a slower tonic component that adapts based on the output of the phasic component. Adaptation in the tonic component frees the phasic component to compensate for further image disparities. Limits of vergence should arise when the tonic component can no longer adapt, but this failure has yet to be observed empirically. We tested the hypothesis that vergence limits would arise when there was evidence of a weakening adaptation in the tonic component.Methods : We adapted the vergence system of 6 subjects using a Wheatstone stereoscope. Binocular eye position was collected with an Eyelink 1000 eyetracker. Subjects binocularly viewed a detailed image of a natural scene. The image was initially presented at zero disparity, and moved laterally in one eye at a rate of 0.5°/s to reach 4° of eccentricity, where it remained for 5 m. Then the image moved in blocks, where each block comprised 1° of movement followed by 5 m of viewing at the new eccentricity. Blocks repeated until subjects experienced diplopia for 75% of a block. The eyetracker was used to calculate the angle between the eyes optical axes, which we term divergence. Phoria was measured every 30 s by calculating divergence when the image in one eye was replaced with a gray field for 5 s. As a control, subjects also viewed the display with one image moving continuously without the 5 m adaptation periods.Results : Subjects were able to fuse the images until eye divergence reached 7.14°, on average. We used phoria to estimate adaptation in the tonic component, with larger phorias indicating less adaptation. Adaptation, as measured by phoria, decreased over successive blocks (linear trend, p < 0.01). In addition, subjects reached a significantly greater divergence with adaptation than in the control condition (5.17°, p = 0.02).Conclusions : Our results support the hypothesis that the amount of vergence normal viewers can produce is limited by adaptation in the tonic component. In earlier blocks, when the tonic component adapted more fully, subjects were able to fuse the images, but in later blocks adaptation of the tonic component lagged behind, and diplopia was experienced. Future work can explore how the tonic component could adapt further, allowing the eyes to experience vergence angles unreachable in normal experience.
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2.
  • McLoon, Linda K., et al. (författare)
  • A continuum of myofibers in adult rabbit extraocular muscle : force, shortening velocity, and patterns of myosin heavy chain colocalization
  • 2011
  • Ingår i: Journal of applied physiology. - Bethesda, Md. : American Physiological Society. - 8750-7587 .- 1522-1601. ; 111:4, s. 1178-1189
  • Tidskriftsartikel (refereegranskat)abstract
    • Extraocular muscle (EOM) myofibers do not fit the traditional fiber typing classifications normally used in noncranial skeletal muscle, in part, due to the complexity of their individual myofibers. With single skinned myofibers isolated from rectus muscles of normal adult rabbits, force and shortening velocity were determined for 220 fibers. Each fiber was examined for myosin heavy chain (MyHC) isoform composition by densitometric analysis of electrophoresis gels. Rectus muscle serial sections were examined for coexpression of eight MyHC isoforms. A continuum was seen in single myofiber shortening velocities as well as force generation, both in absolute force (g) and specific tension (kN/m(2)). Shortening velocity correlated with MyHCIIB, IIA, and I content, the more abundant MyHC isoforms expressed within individual myofibers. Importantly, single fibers with similar or identical shortening velocities expressed significantly different ratios of MyHC isoforms. The vast majority of myofibers in both the orbital and global layers expressed more than one MyHC isoform, with up to six isoforms in single fiber segments. MyHC expression varied significantly and unpredictably along the length of single myofibers. Thus EOM myofibers represent a continuum in their histological and physiological characteristics. This continuum would facilitate fine motor control of eye position, speed, and direction of movement in all positions of gaze and with all types of eye movements-from slow vergence movements to fast saccades. To fully understand how the brain controls eye position and movements, it is critical that this significant EOM myofiber heterogeneity be integrated into hypotheses of oculomotor control.
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3.
  • McLoon, Linda K., et al. (författare)
  • Composition, architecture, and functional implications of the connective tissue network of the extraocular muscles
  • 2018
  • Ingår i: Investigative Ophthalmology and Visual Science. - Rockville : The Association for Research in Vision and Ophthalmology. - 0146-0404 .- 1552-5783. ; 59:1, s. 322-329
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: We examined the pattern and extent of connective tissue distribution in the extraocular muscles (EOMs) and determined the ability of the interconnected connective tissues to disseminate force laterally.Methods: Human EOMs were examined for collagens I, III, IV, and VI; fibronectin; laminin; and elastin using immunohistochemistry. Connective tissue distribution was examined with scanning electron microscopy. Rabbit EOMs were examined for levels of force transmission longitudinally and transversely using in vitro force assessment.Results: Collagens I, III, and VI localized to the endomysium, perimysium, and epimysium. Collagen IV, fibronectin, and laminin localized to the basal lamina surrounding all myofibers. All collagens localized similarly in the orbital and global layers throughout the muscle length. Elastin had the most irregular pattern and ran longitudinally and circumferentially throughout the length of all EOMs. Scanning electron microscopy showed these elements to be extensively interconnected, from endomysium through the perimysium to the epimysium surrounding the whole muscle. In vitro physiology demonstrated force generation in the lateral dimension, presumably through myofascial transmission, which was always proportional to the force generated in the longitudinally oriented muscles.Conclusions: A striking connective tissue matrix interconnects all the myofibers and extends, via perimysial connections, to the epimysium. These interconnections are significant and allow measurable force transmission laterally as well as longitudinally, suggesting that they may contribute to the nonlinear force summation seen in motor unit recording studies. This provides strong evidence that separate compartmental movements are unlikely as no region is independent of the rest of the muscle.
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4.
  • McLoon, Linda K, et al. (författare)
  • Wnt and Extraocular Muscle Sparing in Amyotrophic Lateral Sclerosis
  • 2014
  • Ingår i: Investigative Ophthalmology and Visual Science. - : ARVO, The Association for Reserach in Vision and Ophthalmology. - 0146-0404 .- 1552-5783. ; 55:9, s. 5482-5496
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: The extraocular muscles (EOM) and their motor neurons are spared in amyotrophic lateral sclerosis (ALS). In limb muscle axon retraction from the neuromuscular junctions occurs early in the disease. Wnts, a conserved family of secreted signaling molecules, play a critical role in neuromuscular junction formation. This is the first study to examine Wnt signaling for its potential involvement in maintenance of normal morphology in EOMs in ALS.METHODS: EOM and limb muscle axons, neuromuscular junctions, and myofibers from control, aging, and ALS patients and the SOD1G93A mouse model of ALS were quantified for their expression of Wnt1, Wnt3a, Wnt5a, Wnt7a, and beta-catenin.RESULTS: All four Wnt isoforms were expressed in most axon profiles in all human EOMs. Significantly fewer were positive for Wnt1, Wnt3a, and Wnt7a in the human limb muscles. Similar differential patterns in Wnt myofiber expression was also seen, except for Wnt7a, where expression was elevated. In the SOD1G93A mouse, all 4 Wnt isoforms were significantly decreased in the neuromuscular junctions at the terminal stage compared to age matched controls. Beta-catenin was activated in a subset of myofibers in EOM and limb muscle in all patients.CONCLUSIONS: The differences in Wnt expression in EOM and limb muscle, particularly at the neuromuscular junction level, suggest that they play a role in the pathophysiology of ALS. Collectively, the data support a role for Wnt signaling in the preservation of the EOM in ALS and their dysregulation and the subsequent development of pathology in the ALS limb muscles.
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