Gliosis and ganglion cell death in the developing cat retina during hydrocephalus and after decompression

Williamson, E C; Pearson, Helen; McAllister, James P.

doi:10.1016/0165-3806(92)90102-3

Cited by 12 publications

(5 citation statements)

References 28 publications

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“…Thus, it is speculated that visual acuity, mainly served by the X-cell pathway among various functions of area 17, is disrupted by the hydrocephalus, whereas the detection of moving visual objects may be preserved in that orientation maps relevant to the Y-cell pathway were retained. This interpretation is consistent with that reported earlier in cases of human hydrocephalus (Gaston, 1985;Williamson et al, 1992). Although we did not measure intraocular pressure in our hydrocephalic cats, it is reported that Y-cells exhibited significantly higher tolerance to brief elevation of intraocular pressure than did X-cells in cats (Shou & Zhou, 1989).…”

Section: Vulnerability Of X-pathway In Hydrocephalussupporting

confidence: 93%

“…Thus, it is speculated that visual acuity, mainly served by the X‐cell pathway among various functions of area 17, is disrupted by the hydrocephalus, whereas the detection of moving visual objects may be preserved in that orientation maps relevant to the Y‐cell pathway were retained. This interpretation is consistent with that reported earlier in cases of human hydrocephalus (Gaston, 1985; Williamson et al. , 1992).…”

Section: Discussionmentioning

confidence: 99%

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Preservation of functional architecture in visual cortex of cats with experimentally induced hydrocephalus

Imamura

Tanaka

Ribot

et al. 2006

Eur J of Neuroscience

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We investigated how neural function is preserved or matured in the visual cortex of cats, following the induction of hydrocephalus by kaolin injection. In vivo optical imaging of intrinsic signals in 11-17-week-old hydrocephalic cats revealed orientation maps showing the orderly arrangement of preferred orientations when stimulated by grating stimuli at a low spatial frequency, whereas stimulus-evoked intrinsic signals in response to gratings at a high spatial frequency were often too weak to construct orientation maps. Furthermore, in two of the three hydrocephalic cats, initially deteriorated orientation maps became almost regular maps in the second imaging experiments conducted 8 and 11 weeks, respectively, after the first imaging. This indicates that, despite large structural deformation of the hydrocephalic brain, orientation maps are elaborated sufficiently after the age of 5-6 months, by which time the orientation map formation is usually completed in normal cats. Single unit recording from the decompressed visual cortex revealed that many neurons showed normal orientation selectivity, whereas the binocularity of these neurons was found to be reduced. These results suggested that the deformed visual cortex of hydrocephalic cats exhibits a high plasticity, retaining its functional organization.

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Section: Vulnerability Of X-pathway In Hydrocephalussupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Preservation of functional architecture in visual cortex of cats with experimentally induced hydrocephalus

Imamura

Tanaka

Ribot

et al. 2006

Eur J of Neuroscience

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“…A reduction in the number of ganglion cell axons in the optic nerve was observed in one Nestin-Cre/DG null mouse that was affected by severe hydrocephalus (data not shown). Ganglion cell loss has been previously associated with hydrocephalus (Williamson et al, 1992). This example of optic nerve atrophy was not representative, as no significant difference was observed in the optic nerve cross-sectional area, perimeter, or myelinated axon density of three Nestin-Cre/DG null mice that were not affected by hydrocephalus (Supplemental Figure 7B-E).…”

Section: Resultsmentioning

confidence: 99%

Visual Impairment in the Absence of Dystroglycan

Satz¹,

Philp²,

Nguyen³

et al. 2009

J. Neurosci.

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Ocular involvement in muscular dystrophy ranges from structural defects to abnormal electroretinograms. While the mechanisms underlying the abnormal retinal physiology in patients are not understood, it is thought that ␣-dystroglycan extracellular interactions are critical for normal visual function. Here we show that ␤-dystroglycan anchors dystrophin and the inward rectifying K ϩ channel Kir4.1 at glial endfeet and that disruption of dystrophin and potassium channel clustering in dystroglycan mutant mice is associated with an attenuation of the electroretinogram b-wave. Glial-specific inactivation of dystroglycan or deletion of the cytoplasmic domain of ␤-dystroglycan was sufficient to attenuate the electroretinogram b-wave. Unexpectedly, deletion of the ␤-dystroglycan cytoplasmic domain did not disrupt the laminar structure of the retina. In contrast to the role of ␣-dystroglycan extracellular interactions during early development of the CNS, ␤-dystroglycan intracellular interactions are important for visual function but not the laminar development of the retina.

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“…A third possibility is that the animals were visually impaired. We did not directly test the visual ability of animals, however, the findings of irreversible retinal ganglion cell degeneration in the cat (Williamson et al, 1992) suggests that our animals may not have fully intact vision. We tested the animals in the cued version of the MWM, where the platform location is marked by a cue immediately over the platform.…”

Section: Discussionmentioning

confidence: 99%

Kaolin‐induced ventriculomegaly at weaning produces long‐term learning, memory, and motor deficits in rats

Williams

Braun

Amos‐Kroohs

et al. 2014

Intl J of Devlp Neuroscience

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Ventriculomegaly occurs when there is imbalance between creation and absorption of cerebrospinal fluid (CSF); even when treated, long-term behavioral changes occur. Kaolin injection in the cisterna magna of rats produces an obstruction of CSF outflow and models one type of hydrocephalus. Previous research with this model shows that neonatal onset has mixed effects on Morris water maze (MWM) and motoric performance; we hypothesized that this might be because the severity of ventricular enlargement was not taken into consideration. In the present experiment, rats were injected with kaolin or saline on postnatal day (P)21 and analyzed in subgroups based on Evan's ratios (ER) of the severity of ventricular enlargement at the end of testing to create 4 subgroups from least to most severe: ER0.4–0.5, ER0.51-0.6, ER0.61-0.7, and ER0.71-0.82, respectively. Locomotor activity (dry land and swimming), acoustic startle with prepulse inhibition (PPI), and MWM performance were tested starting on P28 (122 cm maze) and again on P42 (244 cm maze). Kaolin-treated animals weighed significantly less than controls at all times. Differences in locomotor activity were seen at P42 but not P28. On P28 there was an increase in PPI for all but the least severe kaolin-treated group, but no difference at P42 compared with controls. In the MWM at P28, all kaolin-treated groups had longer path lengths than controls, but comparable swim speeds. With the exception of the least severe group, probe trial performance was worse in the kaolin-treated animals. On P42, only the most severely affected kaolin-treated group showed deficits compared with control animals. This group showed no MWM learning and no memory for the platform position during probe trial testing. Swim speed was unaffected, indicating motor deficits were not responsible for impaired learning and memory. These findings indicate that kaolin-induced ventriculomegaly in rats interferes with cognition regardless of the final enlargement of the cerebral ventricles, but final size critically determines whether lasting locomotor, learning, and memory impairments occur.

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Gliosis and ganglion cell death in the developing cat retina during hydrocephalus and after decompression

Cited by 12 publications

References 28 publications

Preservation of functional architecture in visual cortex of cats with experimentally induced hydrocephalus

Preservation of functional architecture in visual cortex of cats with experimentally induced hydrocephalus

Visual Impairment in the Absence of Dystroglycan

Kaolin‐induced ventriculomegaly at weaning produces long‐term learning, memory, and motor deficits in rats

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