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Y H Yücel

Publications and source records attributed to Y H Yücel.

11 recordsLinked to original sources
PubMed2003

Brain changes in glaucoma.

There is evidence that glaucomatous damage extends from retinal ganglion cells to vision centers in the brain. In the lateral geniculate nucleus (LGN), the major relay center between the eye and the visual cortex, neurons should undergo degenerative and/or neurochemical changes in magno-, parvo-, and koniocellular pathways conveying motion, red-green, and blue-yellow information, respectively. Furthermore, in both the LGN and visual cortex in glaucoma, changes in metabolic activity are observed. The study of brain changes in glaucoma may provide new insights into the pathobiology of glaucomatous damage and disease progression, and may stimulate new detection and therapeutic strategies to prevent blindness.

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PubMed2001

Atrophy of relay neurons in magno- and parvocellular layers in the lateral geniculate nucleus in experimental glaucoma.

PURPOSE: To determine whether in glaucoma there is atrophy of relay neurons in magnocellular and/or parvocellular lateral geniculate nucleus (LGN) layers projecting to the visual cortex and to compare the degree of neuronal atrophy in magnocellular layers with that in parvocellular layers. METHODS: Seven cynomolgus monkeys with unilateral experimentally induced glaucoma and five control monkeys were studied. The left LGN neurons in magnocellular layer 1 and parvocellular layers 4 and 6, connected to the right glaucomatous eye were examined. Immunocytochemistry with antibody to parvalbumin was used to specifically label relay neurons connecting to the visual cortex. Neuronal cell body cross-sectional area was estimated using unbiased point-counting methodology. Experimental and control groups were compared using t-tests. Analysis of covariance (ANCOVA) tests were used to compare the percentage of decrease in mean neuronal area between layers 1, 4, and 6, as a function of percentage of optic nerve fiber loss or mean IOP. There was significant correlation between percentage of optic nerve fiber loss and mean IOP. RESULTS: The mean cross-sectional area of relay neurons in magnocellular layer 1 and parvocellular layers 4 and 6 were significantly decreased in glaucoma compared with controls by 28%, 37%, and 45%, respectively. Neuronal area decreased in a linear fashion, with increasing optic nerve fiber loss or increasing mean IOP for layers 1, 4, and 6. The percentage of neuronal shrinkage in each of parvocellular layers 4 and 6, as a function of optic nerve fiber loss (P = 0.05; P = 0.001, respectively) or mean IOP (P = 0.046; P = 0.0008, respectively), was greater than that seen in magnocellular layer 1. CONCLUSIONS: Relay neurons in the LGN, which project to the visual cortex, undergo significant shrinkage in glaucoma, and neurons in parvocellular layers undergo significantly more shrinkage than neurons in magnocellular layers.

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PubMed2000

Loss of neurons in magnocellular and parvocellular layers of the lateral geniculate nucleus in glaucoma.

OBJECTIVES: To determine whether there is loss of lateral geniculate nucleus relay neurons, which convey visual information to the visual cortex, in experimental glaucoma in monkeys. METHOD: Four cynomolgus monkeys with experimentally induced glaucoma in the right eye (referred to as the glaucoma group) and 5 control monkeys were studied. In both groups, the same conditions of fixation, tissue processing, staining, and measurement were used. In each monkey, the left lateral geniculate nucleus target neurons in magnocellular layer 1 and parvocellular layers 4 and 6, connected to the right glaucomatous eye, were studied. Immunocytochemistry with antibody to parvalbumin was used to specifically label relay neurons connecting to the visual cortex. The number of parvalbumin-immunoreactive neurons was estimated using an unbiased 3-dimensional counting method. The t test was used to compare the experimental and control groups. RESULTS: The mean ( SD) number of neurons in mavnocellular layer 1 was significantly decreased in the glaucoma group compared with the control group (20 692 9567 vs 37 687 8017; P = .02). The mean ( SD) number of neurons in parvocellular layers 4 and 6 was significantly decreased in the glaucoma group compared with the control group (100 141 44 906 vs 174 090 39 136; P = .03). Data are given as the mean SD. CONCLUSION: Significant loss of lateral geniculate nucleus relay neurons terminating in the primary visual cortex occurs in the magnocellular and parvocellular layers in an experimental monkey model of glaucoma. CLINICAL RELEVANCE: Knowledge of the fate of neurons in the central visual system may lead to a better understanding of the nature and progression of visual loss in glaucomatous optic neuropathy.

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PubMed1999

Histomorphometric analysis of optic nerve changes in experimental glaucoma.

PURPOSE: To assess relative changes in different tissue components of optic nerve and their relationship to nerve fiber loss in the experimental monkey model of glaucoma. METHODS: Chronic intraocular pressure (IOP) elevation was induced by laser trabeculoplasty in the right eye of eight monkeys (Macaca fascicularis). Both experimental right optic nerves and control left optic nerves were studied. Histomorphometric analysis was performed on optic nerve cross-sections using bright field microscopy with camera lucida. Cross-sectional areas of optic nerve tissue components were estimated by point counting. Nerve fiber density was estimated by unbiased random sampling. Nerve fiber number was calculated by multiplying nerve fiber density with neuroglial area. RESULTS: Varying degrees of nerve fiber loss were seen in eight optic nerves with chronic IOP elevation. More than 50% nerve fiber loss was noted in four of eight experimental optic nerves. In these severely affected optic nerves, total optic nerve area was significantly decreased compared with control optic nerves. Among the optic nerve tissue components, only the ratio of myelinated fiber area to total optic nerve area was significantly decreased. The ratio of extraaxonal area to total optic nerve area was significantly increased, whereas the ratio of interfascicular septal area to total optic nerve area did not change significantly. For all optic nerves, differences in nerve fiber count between control and experimental optic nerves showed the strongest correlation with differences in myelinated fiber area, followed by differences in extraaxonal area and total optic nerve area. CONCLUSION: This histomorphometric study suggests the validity of the experimental monkey model of glaucoma in studying changes occurring in the nonaxonal optic nerve tissue components in human glaucomatous optic neuropathy. Glial scar tissue area was significantly increased in optic nerves with severe glaucomatous damage. Although a decrease in total optic nerve area was observed, among the optic nerve tissue components only myelinated nerve fiber area decreased significantly. Myelinated nerve fiber area also showed the strongest association with nerve fiber loss in experimental glaucoma.

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PubMed1998

Relationship of optic disc topography to optic nerve fiber number in glaucoma.

OBJECTIVE: To assess the relationship between in vivo measurements of optic disc topography and histomorphometric measurements of optic nerve fiber number in glaucoma. METHODS: Both eyes of 10 monkeys (Macaca fascicularis) with laser-induced glaucoma in the right eye were studied. Optic disc topography was measured in vivo with a confocal scanning laser ophthalmoscope. Histomorphometry was performed on optic nerve cross sections using bright-field microscopy with camera lucida. Nerve fiber density was estimated by unbiased random sampling. Nerve fiber number was estimated for each sector by multiplying nerve fiber density with neuroglial area. Nerve fiber count was compared with each of 13 global optic disc topographic parameters. RESULTS: For neuroretinal measurements in the glaucomatous eyes, rim area, retinal nerve fiber layer (RNFL) cross-sectional area, rim volume, and RNFL thickness correlated significantly with optic nerve fiber number. Differences in nerve fiber count between control and glaucomatous optic nerves showed the strongest correlation with differences in mean height contour; this was followed by RNFL cross-sectional area, RNFL thickness, rim volume, and differences in rim area. For cup measurements in the glaucomatous eyes, cup volume below reference, cup area, mean cup depth, the ratio of cup area to disc area, and cup shape correlated significantly with nerve fiber number. Differences in nerve fiber number between control and glaucomatous optic nerves showed the strongest correlation with differences in cup shape; this was followed by mean cup depth, cup volume below reference, the ratio of cup area to disc area, cup area, and differences in cup volume below surface. No association was found between optic nerve fiber number and optic disc area in glaucomatous eyes. CONCLUSIONS: In experimental glaucoma, most optic disc topography measures correlated significantly with optic nerve fiber number. The results of this histomorphometric study support the use of confocal scanning laser ophthalmoscopy to evaluate optic nerve damage in glaucoma.

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PubMed1991

Unilateral pretectal microinjections of SR 95,531, a GABA A antagonist: effects on directional asymmetry of frog monocular OKN.

Monocular eye movements have been studied in frogs using the search coil technique before and after unilateral microinjection of SR 95,531, a GABA A antagonist, into the pretectal nuclei contralateral to the open eye. Before injection, monocular, horizontal optokinetic nystagmus (OKN) in frogs, as in other lower vertebrates, displays a directional asymmetry: the stimulation in the T-N (temporo-nasal) direction is more efficient in evoking OKN than is stimulation in the N-T (naso-temporal) direction. The N-T component is almost absent and displays only slow phases of very low speed. Unilateral SR 95,531 microinjection into the pretectum reversibly decreased the directional asymmetry of monocular horizontal OKN, by strongly increasing the N-T component slow phase velocity while the T-N slow phase velocity remained unchanged. These data show that SR 95,531 injected into the pretectum contralateral to the open eye reversibly decreased the inhibition upon the N-T component of monocular horizontal OKN, which suggests that a pretectal GABAergic system is involved in the directional asymmetry of monocular horizontal OKN in frogs.

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PubMed1990

Directional asymmetry of the horizontal monocular head and eye optokinetic nystagmus: effects of picrotoxin.

Frog monocular eye and head optokinetic nystagmus (OKN) were studied by coil recordings after intravitreal administration of picrotoxin into the closed eye. Before injection, the frog displayed an OKN only for stimulations in the temporo-nasal (T-N) direction. The injection of picrotoxin provoked the appearance of a N-T component of the head and eye OKN: the slow phase velocity gain and the resetting fast phase frequency were strongly and significantly increased. Thus, picrotoxin abolished the directional asymmetry of head and eye OKN, indicating the involvement of GABAergic mechanisms in the inhibition of the N-T component of the monocular eye and head OKN. Picrotoxin administration had an additional effect on the monocular head OKN only, the performances (measured by the velocity gain and the frequency of resetting fast phases) were markedly increased for both directions of stimulation, suggesting an effect of the drug upon the motor output of head movements.

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PubMed1989

Is a retinal input involved in the generation of eye resetting fast phases in the frog eye optokinetic nystagmus?

An intravitreal injection of cis-2,3-piperidine dicarboxylic acid (PDA), a glutamate analog, in one eye only, decreased or even totally suppressed the eye resetting fast phases (ERFPs) of the frog optokinetic nystagmus (OKN) in monocular as in binocular situations. On the opposite, for low drum speeds, the slow phase eye velocity was not affected by PDA. Moreover, it seems that intravitreally injected PDA does not act upon central structures responsible for OKN. Our experiments suggest that a retinal input may be involved in triggering the ERFPs in the OKN.

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PubMed1989

Involvement of ON and OFF retinal channels in the eye and head horizontal optokinetic nystagmus of the frog.

The specific role of ON and OFF retinal information channels in the generation of the horizontal optokinetic nystagmus (OKN) of the frog was studied. Coil recordings of monocular eye and head OKN were obtained before and after intravitreal injection of two drugs that block either ON or OFF channels. The intravitreal injection of 2-amino-4-phosphonobutyrate (APB), a glutamate analog that selectively blocks the ON retinal channel, strongly reduced or even cancelled the monocular OKN of the head and of the eye. The intravitreal injection of another glutamate analog, the cis-2,3-piperidine dicarboxylic acid (PDA) that especially blocks the OFF retinal channel, did not affect the gain velocity of the slow phase of both the horizontal monocular head and eye OKN, for low stimulus velocities. Our results suggest that the retinal ON information channel, but not the OFF channel, is involved in the generation of the slow phase of the OKN of the frog, at least at low drum velocities.

Aminobutyrates↗
PubMed1988

GAD immunoreactivity in pretectal and accessory optic nuclei of the frog mesencephalon.

By an immunocytochemical technique using anti-GAD antibodies, we found a high density of GAD-immunoreactive puncta in the 5 pretectal nuclei and in the nucleus of the basal optic root. These results back up the suggestion that GABAergic modulation of the output of the visual pretectal relay nuclei might underlie the directional asymmetry of the horizontal optokinetic nystagmus and the directional selectivity of pretectal neurons.

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