This review summarizes the current scientific literature concerning the ependymal lining of the cerebral ventricles of the brain with an emphasis on selective barrier function and protective roles for the common ependymal cell. Topics covered include the development, morphology, protein and enzyme expression including reactive changes, and pathology. Some cells lining the neural tube are committed at an early stage to becoming ependymal cells. They serve a secretory function and perhaps act as a cellular/axonal guidance system, particularly during fetal development. In the mature mammalian brain ependymal cells possess the structural and enzymatic characteristics necessary for scavenging and detoxifying a wide variety of substances in the CSF, thus forming a metabolic barrier at the brain-CSF interface.

Background and Purpose-Tumor necrosis factor-␣ (TNF-␣) expression is increased in brain after cerebral ischemia, although little is known about its abundance and role in intracerebral hemorrhage (ICH). A TNF-␣-specific antisense oligodeoxynucleotide (ORF4-PE) was used to study the extent to which TNF-␣ expression influenced neurobehavioral outcomes and brain damage in a collagenase-induced ICH model in rat. Methods-Male Sprague-Dawley rats were anesthetized, and ICH was induced by intrastriatal administration of heparin and collagenase. Immediately before or 3 hours after ICH induction, ORF4-PE was administered directly into the site of ICH. TNF-␣ mRNA and protein levels were measured by reverse transcriptase-polymerase chain reaction and immunoblot analyses. Cell death was measured by terminal deoxynucleotidyl transferase-mediated uridine 5Јtriphosphate-biotin nick end labeling (TUNEL). Neurobehavioral deficits were measured for 4 weeks after ICH. Results-ICH induction (nϭ6) elevated TNF-␣ mRNA and protein levels (PϽ0.01) at 24 hours after the onset of injury compared with sham controls (nϭ6). Immunohistochemical labeling indicated that ICH was accompanied by elevated expression of TNF-␣ in neutrophils, macrophages, and microglia. Administration of ORF4-PE (2.0 nmol) directly into striatal parenchyma, 15 minutes before (nϭ4) or 3 hours after (nϭ6) ICH, decreased levels of TNF-␣ mRNA (PϽ0.001) and protein (PϽ0.01) in the brain tissue surrounding the hematoma compared with animals treated with saline alone (nϭ6). MeanϮSEM striatal cell death (cells per high-powered field) was also reduced in animals receiving ORF4-PE (34.1Ϯ5.0) compared with the saline-treated ICH group (80.3Ϯ7.50) (PϽ0.001). ORF4-PE treatment improved neurobehavioral deficits observed at 24 hours (PϽ0.001) after induction of ICH (nϭ6) compared with the untreated ICH group (nϭ6). This improvement was maintained at 28 days after hemorrhage induction (PϽ0.001). Conclusions-These

To determine the role of the Tat protein of the human immunodeficiency virus type 1 (HIV-1) in the pathogenesis of HIV-1 associated dementia, recombinant Tat was injected intraventricularly as a single or repeated dose into male Sprague-Dawley rats. Histopathological evaluation showed an initial infiltration of neutrophils one day after Tat injection, followed by macrophages and lymphocytes by 7 days. Tat-injected brains also exhibited astrocytosis, apoptotic cells, and ventricular enlargement 7 days following the last injection. Nuclear magnetic resonance spectroscopic analysis of tissue extracts of hippocampi from Tat-injected rats showed a decrease in the glutamate/g aminobutyric acid ratio. We conclude that the transient extracellular exposure of the central nervous system to Tat protein of HIV can cause a cascade of events leading to the influx of inflammatory cells, glial cell activation, and neurotoxicity.