Subject(s)
Intracranial Hypertension , Pre-Eclampsia , Eye , Female , Humans , Intracranial Pressure , Pregnancy , UltrasonographyABSTRACT
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ABSTRACT
Photoreceptor degeneration is followed by significant morphological changes in the second-order retinal neurons in humans and in several genetic animal models. However, it is not clear whether similar changes occur when photoreceptor degeneration is induced nongenetically, raising the question whether these changes are a general effect of deafferentation independent of the cause of degeneration. We addressed this by inducing selective photoreceptor degeneration with N-methyl-N-nitrosourea (MNU) and studying its effects on inner retinal neurons in a mouse for up to 3 months, using immunocytochemistry and iontophoretic labeling. To develop objective measures of photoreceptor degeneration and of retinal remodeling, we measured several retinal proteins using immunoblot analysis, and quantified gross visual ability of the animal in a visual cliff test. The MNU-induced progressive degeneration of rods and cones was associated with declining levels of postsynaptic density 95 protein in the retina, and with deteriorating visual performance of the animal. Müller glial cells showed enhanced reactivity for glial fibrillary acidic protein as demonstrated by immunocytochemistry, which also reflected in increased levels of the protein as demonstrated by immunoblotting. Horizontal cells and rod bipolar cells progressively lost their dendritic processes, which correlated with a slight decline in the levels of calbindin and protein kinase C alpha respectively. Horizontal cell axons, immunoreactive for nonphosphorylated neurofilaments, showed sprouting into the inner nuclear layer. Ganglion cells and their synaptic inputs, probed by immunolocalizing beta-III-tubulin, neurofilaments, bassoon and synaptophysin, appeared to be unaffected. These results demonstrate that MNU-induced photoreceptor degeneration leads to retinal remodeling similar to that observed in genetic models, suggesting that the remodeling does not depend on the etiopathology that underlies photoreceptor degeneration.
Subject(s)
Alkylating Agents , Methylnitrosourea , Nerve Degeneration/chemically induced , Nerve Regeneration/physiology , Photoreceptor Cells, Vertebrate/pathology , Retinal Degeneration/chemically induced , Animals , Disease Models, Animal , Immunohistochemistry , Male , Mice , Mice, Inbred C57BL , Nerve Degeneration/pathology , Nerve Degeneration/physiopathology , Neuronal Plasticity , Photoreceptor Cells, Vertebrate/drug effects , Photoreceptor Cells, Vertebrate/physiology , Retina/drug effects , Retina/pathology , Retina/physiology , Retinal Degeneration/pathology , Retinal Degeneration/physiopathology , Spatial Behavior , Visual Acuity/drug effectsABSTRACT
BACKGROUND AND PURPOSE: Before the advent of MR imaging, intraventricular cysts were difficult to diagnose noninvasively. Among the invasive procedures used were contrast ventriculography and CT ventriculography. MR imaging, with its multiplanar imaging capabilities, excellent depiction of tissue contrast, and versatile parameters, is an important tool in the assessment of intraventricular cystic lesions. We investigated the role of three-dimensional constructive interference in steady state (3D-CISS) MR sequences in the evaluation of intraventricular cysticercal cysts. METHODS: The study group comprised 11 patients with intraventricular cysticercal cysts. MR studies included spin-echo (SE) T1-weighted, turbo-SE T2-weighted, and 3D-CISS sequences. All images were obtained on a superconducting 1.5-T MR unit. The routine and 3D-CISS sequences were reviewed and interpreted separately by two neuroradiologists. RESULTS: All patients underwent surgery for excision of intraventricular cysticercal cysts. Eight patients had cysts in the fourth ventricle, two in the lateral ventricle, and one in the third ventricle. SE T1-weighted images showed the cystic wall in nine cases, the scolex in four, and the cystic fluid in two. Turbo-SE T2-weighted images showed the cystic wall and scolex in three and four cases, respectively. The routine sequences did not show the scolex, cystic wall, or cystic fluid together in any of the 11 patients. 3D-CISS images showed the scolex in all 11 patients and the cystic wall and cystic fluid in eight patients each. In seven of the 11 patients, 3D-CISS images showed the scolex, cystic wall, and fluid together. CONCLUSION: The 3D-CISS sequence is more sensitive and specific than routine SE sequences in the diagnosis of intraventricular cysticercal cysts.
