Hydrocephalus is a common medical condition characterized by abnormalities in the secretion,circulation or resorption of cerebrospinal fluid (CSF), resulting in ventricular dilatation. The pathogenetic mechanism for the hydrocephalus is attributed to: the overproduction of CSF by the choroid plexus; the defect in CSF absorption and obstruction of CSF flow in the cerebral ventricles. However, the underlying etiology is poorly understood. With the development of genetic engineering, a growing body of evidence indicates that genetic factors play an essential role in the pathogenesis of hydrocephalus. It is the aim of this review to summarize these findings.
Animals ; Cerebral Ventricles ; pathology ; Disease Models, Animal ; Hydrocephalus ; genetics ; pathology ; Mice ; Mice, Knockout

OBJECTIVETo examine the proliferation of the neural progenitor cells in the subventricular zone (SVZ) and around the hematoma after intracerebral hemorrhage (ICH) in adult rats.

METHODSICH was induced by stereotactic injection of type VII collagenase into the corpus striatum of adult rats, followed by pulse or continuous intrapenitoneal injection of bromodeoxyuridine (Brdu) to label the proliferating cells. The rats were sacrificed on days 2, 7, 14 and 28 following the ICH for immunohistochemistry of the tissues in the SVZ and around the hemotoma to determine the number of Brdu- immunoreactive cells.

RESULTSWith pulse Brdu labeling, a significant increase in the number of Brdu-immunoreactive cells in the ipsilateral and contralateral tissues in the SVZ and around the hematoma was observed 2-14 days, and the cell number reached the maximum on day 7 after ICH as compared with that of the sham-operated group. With continuous Brdu injection, the increase was observed on day 14 after ICH, and till day 28, the Brdu-immunoreactive cells in the SVZ decreased to the control level, but some positive cells still persisted in the tissues around the hematoma.

CONCLUSIONICH induces transient and regional increase in the cell proliferation in the ipilateral and contraletral SVZ and tissues around the hematoma, and the proliferating cells in the SVZ may migrate towards the hematoma area.

Animals ; Cell Proliferation ; Cerebral Hemorrhage ; pathology ; Cerebral Ventricles ; pathology ; Hematoma ; pathology ; Male ; Neurons ; pathology ; Rats ; Rats, Sprague-Dawley ; Stem Cells ; pathology

OBJECTIVE: To investigate the relationship between behavioral changes and cell proliferation in subventricular zone (SVZ) after intracerebral hemorrhage (ICH) in adult rats. METHODS: Forty male Sprague-Dawley rats were randomly assigned into a behavioral test group (n = 19) and a bromodeoxyuridine (Brdu) immunohistochemical staining group (n = 21). ICH was induced by stereotactial injection of collagenase type VII into straitum. Proliferating cells were labeled by injection intrapenitoneally of bromodeoxyuridine in a pulse protocal. Rats were killed on day 2, 7, 14, and 28 after the ICH. Behavioral test and bromodeoxyuridine immunohistochemical staining were performed.Behavioral change was tested by forelimb placing test, Berderson's grade and corner turn test in rats. Cell counting of bromodeoxyuridine immunoreactive cells in SVZ was performed. RESULTS: There were marked neurological deficits by day 2 after the ICH, with progressive recovery of function over 4 weeks. A significant increase in the number of bromodeoxyuridine immunoreactive cells in the ipsilateral and cortralateral SVZ was observed from 2 to 14 days with a peak at day 7 after the ICH compared with the sham group.The bromodeoxyuridine immunoreactive cells decreased to control level 28 days after the ICH. CONCLUSION Proliferation of cells in SVZ corresponds well with behavioral recovery after the ICH, which indicates SVZ cells may be involved in the repairing process after the ICH.
Animals ; Behavior, Animal ; physiology ; Cell Proliferation ; Cerebral Ventricles ; pathology ; Intracranial Hemorrhages ; pathology ; physiopathology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Chordoid glioma is a rare low grade tumor typically located in the third ventricle. Although a chordoid glioma can arise from ventricle with tumor cells having features of ependymal differentiation, intraventricular dissemination has not been reported. Here we report a case of a patient with third ventricular chordoid glioma and intraventricular dissemination in the lateral and fourth ventricles. We described the perfusion MR imaging features of our case different from a previous report.
Adult ; Cerebral Ventricle Neoplasms/diagnosis/pathology/*secondary ; Fourth Ventricle/*pathology ; Glioma/diagnosis/*pathology ; Humans ; Lateral Ventricles/*pathology ; Magnetic Resonance Imaging/methods ; Male ; Third Ventricle/*pathology

Adult ; Cerebral Ventricle Neoplasms ; diagnosis ; metabolism ; Diagnosis, Differential ; Glial Fibrillary Acidic Protein ; analysis ; Humans ; Immunohistochemistry ; Lateral Ventricles ; chemistry ; pathology ; Male

The ultrastructural changes of the wall of the fourth ventricular foramina following intraventricular autogenous blood infusion present four meaningful findings for the patho-genesis of secondary hydrocephalus. Using the transmission and scanning electron microscopy (TEM and SEM), it has found that minimal to marked separation of the intercellular cleft coincided with the intra-and intercellular vacuolation and swelling of the glial fibers in the subependymal glial sheath by the 7th day of blood infusion. A f1attening of the contours of the ependymal cells and their nuclei was noted under the TEM and a seperation of ependymal cells was pronounced under the SEM during the period between the 28th and 42nd day. Ultrastructural changes of the ependymal cells correlated with the time factor and not with the blood volume infused. The supraependymal cells (SEC) seen on the ventricular surface were indicative of neuron-like structure rather than macrophages.
Animal ; Blood Transfusion* ; Cats ; Cerebral Ventricles/ultrastructure* ; Comparative Study ; Female ; Hydrocephalus/pathology ; Male ; Microscopy, Electron ; Microscopy, Electron, Scanning

OBJECTIVETo investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction.

METHODSCerebral infarction models of rats were established and the dynamic expression of bromodeoxyuridine (BrdU), BrdU/polysialylated neural cell adhesion molecule (PSA-NCAM) were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark dividing neural stem cells. PSA-NCAM was used to mark the plasticity of neural stem cells.

RESULTSCompared with controls, the number of BrdU-positive cells in the subventricular zone (SVZ) and hippocampus increased significantly at 1st day after cerebral infarction (P < 0.05), reached maximum at 7th day, decreased markedly at 14th day, but it was still elevated compared with that of the controls (P < 0.05). The number of BrdU-labeled with PSA-NCAM-positive cells increased significantly at 7th day (P < 0.05), reached maximum at 14th day, markedly decreased at 28th day, but it was still elevated compared with that of the controls (P < 0.05). It was equal to 60% of the number of BrdU-positive cells in the same period.

CONCLUSIONCerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.

Animals ; Bromodeoxyuridine ; metabolism ; Cell Proliferation ; Cerebral Infarction ; metabolism ; pathology ; Cerebral Ventricles ; pathology ; Hippocampus ; pathology ; Male ; Neural Cell Adhesion Molecule L1 ; metabolism ; Neuronal Plasticity ; Neurons ; metabolism ; pathology ; Rats ; Rats, Wistar ; Sialic Acids ; metabolism ; Stem Cells ; metabolism ; pathology

OBJECTIVETo study the effect of quercetin on the proliferation of neural stem cells in the subventricular zone (SVZ) of rats after focal cerebral ischemia.

METHODSAn adult rat model of middle cerebral artery occlusion (MCAO) model was established by placement of an intraluminal filament at the origin of the MCA. Quercetin was administered intraperitoneally in the rats at a dose of 50 mg/kg every 3 days starting at 6 h after MCAO, and BrdU (50 mg/kg daily) was also injected intraperitoneally starting at 4 h after MCAO. BrdU-positive cells in the SVZ were counted at 7, 14 and 21 days after MCAO.

RESULTSCompared with the sham-operated group, the rats in the ischemic model group showed significantly increased BrdU-positive cells in the ipsilateral SVZ 7 days after MCAO, reaching the peak level on day 14 and beginning to decrease on day 21 (P<0.05). The number of ipsilateral BrdU-positive cells in quercetin group was significantly greater than that in the model group on days 7, 14 and 21 (P<0.05), and maintained the high level on day 21.

CONCLUSIONQuercetin can maintain a high level of neural stem cell proliferation in the SVZ after focal cerebral ischemia in adult rats.

Animals ; Brain Ischemia ; pathology ; physiopathology ; Cell Proliferation ; drug effects ; Cerebral Ventricles ; pathology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Male ; Neural Stem Cells ; cytology ; Quercetin ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology

AIMTo investigate whether the selective AT1 receptor antagonist irbesartan exerts neuroprotective effect on focal cerebral ischemia in normotensive rats.

METHODSCerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion, with the monitoring of laser Doppler flowmetry. To avoid the interaction with peripheral AT1 receptors, irbesartan was infused intracerebroventricularly (ICV) at a dose which effectively inhibited brain- but not vascular AT1 receptors. Neurological status was evaluated daily after MCAO. Rats were killed and brain samples were collected for the measurement of infarct size and immunohistochemical evaluation of apoptosis by deoxynucleotidyltransferase-mediated biotinylated UTP nick end labeling (TUNEL) and expression of activated Caspase-3 and the cleavage fragment of poly (ADP-ribose) polymerase (PARP).

RESULTSTreatment with irbesartan improved significantly the neurobehavioral functions after cerebral ischemia. The infarct size was reduced about 42% on day 7 after MCAO (P < 0.05). Meanwhile,irbesartan treatment significantly decreased the number of TUNEL-positive cells in the penumbra. The expression of activated Caspase-3 and the downstream cleavage fragment of poly (ADP-ribose) polymerase in the penumbra were also inhibited by irbesartan therapy on day 3 after transient cerebral ischemia.

CONCLUSIONAngiotensin AT1 receptor antagonist exhibits neuroprotection against transient cerebral ischemia in the brain. The neuroprotective effects in ischemic tissue may be associated with its inhibition of apoptotic cell death in the penumbra.

Angiotensin Receptor Antagonists ; pharmacology ; Animals ; Biphenyl Compounds ; pharmacology ; Cerebral Infarction ; pathology ; Ischemic Attack, Transient ; drug therapy ; pathology ; Lateral Ventricles ; Male ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Wistar ; Tetrazoles ; pharmacology

OBJECTIVETo investigate the effects of hypoxia-ischemia (HI) on different neural cells and their survival in subventricular zone (SVZ) of human fetus in mid trimester of pregnancy and thus to explore the pathogenesis of hypoxic-ischemic brain damage on the cellular level.

METHODSAcutely dissociated SVZ cells, prepared from five fetuses of human embryos aborted voluntarily at 17 to 22 weeks of gestational age, were cultured for a short time separately under HI (HI group) and normal condition (control group). HI injury was simulated by oxygen/glucose deprivation (OGD) and the dead cells were counted by staining with Trypan blue. The injury was evaluated by the survival rate before culturing. After culturing, all of the neural cells of SVZ, including neural stem cells (NSCs), neurons, astrocytes, oligodendrocyte progenitors and microglia cells were recognized separately by their special marker nestin, microtubule associated proteins 2 (MAP2), glial fibrillary acidic protein (GFAP), platelet derived growth factor receptor alpha (PDGFRalpha) and ricinus communis agglutinin (RCA120) with immunofluorescence cytochemistry. At the same time, all cell nuclei were stained with bisbenzimide. The percentages of SVZ cells were calculated and compared between HI and control groups.

RESULTSThe survival rate of HI SVZ cells, (63.41 +/- 0.06) percent, was much lower than that of control (98.9 +/- 0.01) percent (P < 0.001). The result indicated that SVZ cells were damaged obviously by HI. After culturing shortly the highest proportion of cells in HI group was astrocytes (56.48 +/- 0.03) percent, followed by NSCs (22.47 +/- 0.03) percent, and the lowest was oligodendrocyte progenitors. But in control group, the neurons accounted for (48.81 +/- 0.03) percent and astrocytes (32.31 +/- 0.03) percent, while the lowest was microglia cells.

CONCLUSIONSThere were NSCs, neurons, astrocytes, oligodendrocyte progenitors and microglial cells in SVZ of mid trimester of pregnancy. They were sensitive to HI and their survival rates were different: the NSCs and astrocytes showed higher survival rate than neurons and oligodendrocyte progenitors.

Cell Differentiation ; Cell Survival ; Cells, Cultured ; Cerebral Ventricles ; Female ; Fetus ; cytology ; pathology ; Humans ; Hypoxia-Ischemia, Brain ; pathology ; Neurons ; cytology ; Pregnancy ; Pregnancy Trimester, Second