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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We attempted to develop a method for investigating impairment of synaptogenesis quantitatively involving measurement of the fluorescence intensity emitted by immunohistochemically stained rat brain using a monoclonal antibody (Mab 171B5) against a synaptic vesicle protein (SVP-38). We applied this method to congenitally hydrocephalic and non-hydrocephalic brains of HTX-rats, and compared the postnatal changes in the fluorescence intensity in the molecular layer of the cerebral cortex. In non-hydrocephalic HTX-rats, the fluorescence intensity remained nearly unchanged from the 1st to 7th postnatal day and then increased at an almost linear rate until the 21st postnatal day, when it reached 4.5 times the value on the 7th postnatal day. The increase thereafter was gradual until the 28th postnatal day. In hydrocephalic HTX-rats, the fluorescence intensity increased nearly in parallel with that in non-hydrocephalic HTX-rats up to the 21st postnatal day. On the 28th postnatal day, the fluorescence intensity showed a marked reduction (P less than 0.01). This finding indicates that despite the presence of continuous pressure due to progressive ventricular dilatation after birth, synaptogenesis in the cerebral cortex may be relatively resilient.
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PMID:Cortical synaptogenesis in congenitally hydrocephalic HTX-rats using monoclonal anti-synaptic vesicle protein antibody. 137 82

To investigate the mechanism of cystic cavity formation in the cerebral white matter of the HTX rat, a strain with inherited hydrocephalus, the authors carried out a histopathological study of the brain in pups from birth to postnatal day (P) 26. Cystic cavities were formed in the cerebral white matter on the lateral side of the basal ganglia of all HTX rats with moderate to severe ventricular dilatation and, additionally, in the white matter beneath the paramedian cortex in advanced cases at P10-26. In the initial stage of cyst formation, disarrangement of the ependymal cell layer and spongy alteration of the white matter took place in pups between P1 and P7. The ependymal disarrangement involved disruption and flattening of the ependymal cells, which were often devoid of microvilli, cilia and intercellular junctional complexes. The spongy state was due to expansion of the extracellular space and multiple microcyst formation with fluid accumulation in the early stage, and large cystic cavities in the advanced stage. The cerebrospinal fluid (CSF) in the ventricle communicated with the fluid in the cystic cavities via the disarranged ependymal cell layer. The ependymal damage was more prominent at the lateral wall of the posterior horn than at the anterior horn of the lateral ventricles. These cavities were demarcated by reactive glial cells in the advanced stage. However, the cavities enlarged in accordance with progressive dilatation of the lateral ventricles during postnatal development.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histopathology of cystic cavities in the cerebral white matter of HTX rats with inherited hydrocephalus. 169 91

HTX rat, a congenital hydrocephalic strain, develops ventricular dilatation and cystic cavities in the cerebral white matter after birth. To investigate the reactive changes in glial cells around these cavities, immunohistochemical staining for glial fibrillary acidic protein (GFAP), a specific marker protein of astrocytes, and bromodeoxyuridine (BrdU), a thymidine analogue, was carried out on 107 Wistar and HTX rat brains from birth to postnatal day (P) 26. Animals were divided into three groups: Group A, Wistar rats as normal controls; Group B, HTX rats with a normal structure or only mild ventricular dilatation without any lesion in the white matter; and Group C, HTX rats with severe ventricular dilatation and cyst formation in the white matter. Group B rats showed similar development of GFAP-positive (GFAP+) cells to that in Group A rats, both morphologically and quantitatively. On the other hand, Group C rats showed definite structural changes in GFAP+ cells around the cystic cavities from P5. These included enriched cytoplasm and thickened cell processes with increased GFAP expression, and enveloped most cyst walls from P10. However, quantitative examination of the percentage of GFAP+ cells in Group C rats showed a similar developmental profile to those in Group A and B rats. Furthermore, the labeling index of BrdU-positive cells, indicating S-phase cells, in the white matter in Group C rats showed a similar decreasing pattern to that in Group A and B rats from P1 to P26.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of GFAP-positive cells and reactive changes associated with cystic lesions in HTX rat brain. 170 53

The purpose of the present study is to examine the blood-brain barrier in brain of congenital hydrocephalus HTX rats. We investigated the rat brain from postnatal day 1 to 44 using light and electron microscopy and immunohistochemical methods with monoclonal anti-blood-brain barrier (BBB) antibody. HTX rats developed hydrocephalus at 1-2 days after birth. Most rats succumbed to brain changes within 4-5 weeks. Among 136 HTX rats examined, 45 rats succumbed within 1 week after birth, 29 rats between 1-2 weeks, and 4 rats 27-44 days after birth. Out of 88 hydrocephalic rats 54 showed a marked ventricular dilatation, and 34 showed a mild dilatation. Dilatation of lateral ventricles was mild in the rats at 1-2 days after birth, but 3-14-day-old rats showed moderate or marked dilatation. 15-30 days after birth the rats developed mostly marked dilatation of lateral ventricles and third ventricle. Lateral ventricles and third ventricle showed a symmetric dilatation, but ependymal cell layers were well preserved. Aqueduct exhibited no dilatation in any rat. There were spongy appearances and cystic cavities in the white matter around the lateral ventricles. There were glial fibers and capillaries across the cystic cavities. Cystic lesions were also found in the deep subcortical white matter, consisting of spongy changes with extended extracellular spaces and microcysts in the white matter. Immunohistochemically, the anti-BBB reactivity in the normal control rats was at first weak at 2 weeks after birth and increased with the course of development, prominently 4 weeks after birth. Three- and four-week-old HTX rats with hydrocephalus showed moderate positive anti-BBB reaction in the cerebral cortex, the basal ganglia, and around the aqueduct but only a very weak reaction in the deep subcortical white matter and in the subependymal area of lateral ventricles. Laminin immunoreactivity was not different in the capillaries of hydrocephalic brain as compared with normal brain. Electron microscopically, tight junctions were well formed between endothelial cells of capillaries in the subcortical white matter. Occasionally capillaries with partial defect of basal membrane could be found, where the cytoplasm of endothelial cell was protruding between pericytic cytoplasm. Swelling of astrocytic end-feet were found around the microvessels. The results suggest that at the site of the lesion there is underdevelopment or immaturity of the blood-brain barrier.
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PMID:Immunohistochemical study on blood-brain barrier in congenitally hydrocephalic HTX rat brain. 782 77

HTX rats with congenital hydrocephalus that survived for more than 2 months are termed spontaneously arrested hydrocephalic rats. These rats showed impairment in learning, a reverse light-dark discrimination task in a Y-maze. A clear relationship between learning impairment and ventricular dilatation was observed in spontaneously arrested hydrocephalic animals. The usefulness and limitations of HTX-rats as an animal model of spontaneously arrested hydrocephalus are discussed.
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PMID:A rat model of spontaneously arrested hydrocephalus. A behavioural study. 920 53

Congenitally hydrocephalic HTX rats develop ventricular dilatation with extensive damage of the cerebral white matter. Recently, we have reported that neuronal cell death also occurs in the thalamus of HTX rats. To investigate the mechanism underlying this thalamic degeneration in these animals, we carried out a histopathological study of the brain at different phases of postnatal development. Eosinophilic neurons with condensed chromatin or fragmented nuclei were observed in the thalamus from postnatal day 17 onward. The incidence of cell death in the thalamus increased with the progression of hydrocephalus. Ultrastructurally, thalamic neurons occasionally had apoptotic features including nuclear chromatin condensation and marginalization. Immunohistochemically, single-stranded DNA-positive neuronal nuclei were found in the thalamus. They were also positively stained with the TUNEL method. Marked loss of myelin and axons with many TUNEL-positive oligodendrocytes were found in the cerebral white matter. These findings suggest that the neuronal cell death observed in the thalamus in hydrocephalic HTX rats is retrograde degeneration due to extensive damage of axons in the cerebral white matter and that the thalamic retrograde degeneration is attributable to apoptotic cell death.
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PMID:Thalamic retrograde degeneration in the congenitally hydrocephalic rat is attributable to apoptotic cell death. 1241 58