OBJECTIVETo probe into the morphological and histological characteristics of the telencephalon of Onychodactylus fischeri, and to enrich the comparable neurobiology.

METHODHE-staining method was used to describe the characters of the telencephalon of Onychodactylus fischeri.

RESULTSThe olfactory bulb of Onychodactylus fischeri locates in the rastral and lateral to the cerebral hemisphere, and six distinct layers can be identified from the lateral to the medial, quite similar to Batrachuperus tibetanus and Hynobius leechii. In the cerebrum, the primordial hippocampus developed better than the primordial piriform. The former belongs to archipallium and the latter is paleopallium. Ventral to the primordial hippocampus there is a septal area which cannot be divided into medial and lateral parts. In the ventrical wall, there is neither medial limiting sulcus nor lateral limiting sulcus to separate the primordial hippocampus and the septal area, or the primordial piriform and the corpus striatum. The corpus striatum of Onychodactylus fischeri is paleostriatum. There is choroids plexus anterior in the lateral ventricle. The cell group that located at two sides of the third ventricle is the amygdale. Besides, the shape and size of neurons within the telencephalon are poorly differentiated.

CONCLUSIONOnychodactylus fischeri is a relatively primitive type in the amphibian. The present data will help us to further understand the nerve system of tailed amphibian.

Animals ; Telencephalon ; cytology ; Urodela ; anatomy & histology

Holoprosencephaly is a developmental malformation complex of forebrain and midface which arises from incomplete cleavage of the embryonic forebrain. It is subdivided into alobar, semilobar and lobar types based on the degree of growth disturbance within the anterior wall of the telencephalon, particularly in the midline. Cyclopia is the most severe form of alobar holoprosencephaly presenting a single median eye and a blind-ending proboscis usually located above the eye. We report a case of alobar holoprosencephaly with cyclopia and proboscis in premature infant.
Holoprosencephaly* ; Humans ; Infant, Newborn ; Infant, Premature ; Prosencephalon ; Telencephalon

No abstract available.
Animals ; Brain* ; Diencephalon* ; In Situ Hybridization* ; Rats* ; RNA, Messenger* ; Somatostatin* ; Telencephalon*

We have studied morphologic characteristics and apoptosis on the fetal brain of the trisomy 16 mouse, a model for human trisomy 21 syndrome. This study was based on serial sections of the whole brain from a sample of sixteen trisomy 16 mice and forty-six age-matched control littermates from embryonic day (ED) 12 to ED 18. Trisomy 16 brains showed a reduction of telencephalic size and abnormal cortical development. At ED 13 trisomy 16 and control brains appeared similar. By ED 14 difference in the cortical thickness and telencephalic growth became evident, and by ED 16 a marked size difference had developed between the trisomy 16 and control brains. By ED 18, however, the thickness of the trisomy 16 cortex had increased considerably and was not significantly different with respect to the thickness and cross-sectional areas of the pallium and its constituent cortical layers. The cell density of the trisomy 16 cortex had persistently decreased before ED 17, when the cell density of control and trisomy 16 corteces was similar within each layer. At ED 18 cell density of trisomy 16 cortex in each layer increased. There was inverse relationship between a number of TUNEL positive apoptotic cells and cell density in the trisomy 16 brains. Our results suggest that developmental abnormalities of the trisomy 16 brain indicated developmental delay of the telencephalon growth, which may be caused by apoptosis rather than by a proliferation defect.
Animals ; Apoptosis* ; Brain* ; Cell Count ; Down Syndrome ; Humans ; In Situ Nick-End Labeling ; Mice* ; Telencephalon ; Trisomy*

Foxg1 (previously named BF1) is a winged-helix transcription factor with restricted expression pattern in the telencephalic neuroepithelium of the neural tube and in the anterior half of the developing optic vesicle. Previous studies have shown that the targeted disruption of the Foxg1 gene leads to hypoplasia of the cerebral hemispheres with severe defect in the structures of the ventral telencephalon. To further investigate the molecular mechanisms by which Foxg1 plays essential roles during brain development, we have adopted a strategy to isolate genes whose expression changes immediately after introduction of Foxg1 in cultured neural precursor cell line, HiB5. Here, we report that seventeen genes were isolated by ordered differential displays that are up-regulated by over-expression of Foxg1, in cultured neuronal precursor cells. By nucleotide sequence comparison to known genes in the GeneBank database, we find that nine of these clones represent novel genes whose DNA sequences have not been reported. The results suggest that these genes are closely related to developmental regulation of Foxg1.
Animals ; Base Sequence ; Brain ; Cell Line ; Cerebrum ; Clone Cells ; Neural Tube ; Neurons ; Rats ; Stem Cells ; Telencephalon ; Transcription Factors

Cerebrum ; pathology ; physiopathology ; Congenital Abnormalities ; physiopathology ; Humans ; Infant, Newborn ; Male ; Neonatology ; Osteopetrosis ; complications ; physiopathology ; Research Report ; Telencephalon ; abnormalities

BACKGROUNDThere have been no detailed reports of the three-dimensional structure and the relationship between the external and internal vascularizations observed successively for a long duration in the rat fetus, although many authors have studied the vascular morphology of the developing brain. This study examined the three-dimensional structure of both the external and internal vascularizations of the prenatal rat telencephalon from embryonic days 12 (E12) to 20 (E20).

METHODA microvascular casting method for scanning electron microscopy (SEM) was used in this study, along with vascular staining using gold-gelatin solution-autometallography (GGS-AMG) after intravascular injection of colloidal gold, as well as hematoxylin-eosin (HE) staining for paraffin embedded specimens.

RESULTSIn GGS-AMG stains, E16 fetuses had a few short perforating cortical blood vessels (SPCVs); E17 fetuses had long perforating cortico-medullary vessels (LPCVs). Older fetuses had specific patterns of vascular networks in the cortex and the deeper subcortical part of the telencephalon. In the cortex, fine longitudinal blood vessels were connected by transverse channels. The deep telencephalon had fine blood vessels running in all directions. Using SEM, the external vascularization was already visible in E12 fetuses as arborizations of arterial branches, forming a mesh of fine vascular networks covering the telencephalon. A coralliform fine venous plexus was observed in the external vascularization of E16 fetuses. There were ring-like anastomoses and bud-like protrusions in the network of small blood vessels, most likely the angiogenesis of fetal vessels. From E12 to E16, an immature and incomplete internal vascularization began to appear. There were short blood vessels with ballooned terminals branching from the external vascularization. They penetrated the brain tissue to form networks in the superficial layer, comparable to SPCVs. In E17 to E20 fetuses, tortuous venous branches, straight arterial blood vessels, and a fine network of small blood vessels formed the external vascularization. There were fewer arterial than venous branches connecting to the fine networks of small blood vessels. LPCVs were noted at E17, at the time the white matter emerged. They branched from the external vascularization, and perpendicularly penetrated the brain surface, traversing the cortical plate, and entering into the deep brain. At E17, arterial and venous blood vessels could be clearly distinguished in the external vascularization. At E20, the cortex and white matter contained specific arrangements of networks of fine blood vessels, as seen by GGS-AMG staining.

CONCLUSIONThese findings show that the development of both the external and internal vascularization follows the development of the telencephalon. In particular, the emergence of the cortical plate and white matter on E16 and E17 influence the development of both the internal and the external vascularization. The laminal arrangement of blood vessels was not observed corresponding to the respective laminal neuronal layers.

Animals ; Blood Vessels ; embryology ; ultrastructure ; Embryo, Mammalian ; Fetus ; Microscopy, Electron, Scanning ; Rats ; Rats, Wistar ; Telencephalon ; blood supply

OBJECTIVETo study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium.

METHODSSixty BALB/c mice were divided randomly into four groups with different drinking water: control group (tap water, NC), excess iodine group (3000 microg/L I, EL +), supplementing selenium group (200 microg/L Se, Se +) and the excess iodine plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression level of neurogranin in filial cerebrum was measured by immunohistochemistry and Western blot.

RESULTSSerum T4 level in EI (68.78 +/- 11.10 nmol/ L) + was lower significantly than that in NC (100.85 +/- 11.47 nmol/ L) and EI + Se + (93.15 +/- 12.10 nmol/ L) on postnatal day 14. Western blot analysis showed that the relative level of neurogranin in EI + (0.621 +/- 0.041) was lower than that in NC (0.841 +/- 0.039) and EI + Se + (0.781 +/- 0.029) on postnatal day 14 (P < 0.05). No significant difference in serum T4 and neurogranin level between four groups on postnatal day 28.

CONCLUSIONExcess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.

Animals ; Female ; Iodine ; adverse effects ; Male ; Mice ; Mice, Inbred BALB C ; Neurogranin ; biosynthesis ; Selenium ; pharmacology ; Telencephalon ; metabolism ; Thyroxine ; blood ; Triiodothyronine ; blood

BACKGROUND: Recent increases in use of sevoflurane have made active researches on its effects in the cerebral metabolism. However, no specific data on brain glucose metabolism has been reported from human study. We compared the brain glucose metabolism during sevoflurane anesthesia with that of propofol anesthesia using positron emission tomography (PET) in the same human volunteers. METHODS: PET scan was performed two times at intervals of one week in each eight volunteers. One scan was performed in sevoflurane anesthesia, and the other was performed in propofol anesthesia. Each was titrated to the point of unconsciousness. The scan was obtained by the 18fluorodeoxyglucose technique. Relative cerebral glucose metabolic rate (rCMRg) was assessed with statistical parametric mapping. RESULTS: The regions of decreased rCMRg during sevoflurane aneshesia were the visual cortex, posterior parietal association area, primary somatosensory area, and premotor area. During propofol anesthesia the decreased regions were the visual inferotemporal area and prefrontal association area in addition to those area of sevoflurane anesthesia. The increased regions were the partial prefrontal association area, basal ganglia, cingulate, olfactory-limbic cortex, midbrain, and pons during sevoflurane anesthesia, and the primary motor area, insula, thalamus, medulla along with those area of sevoflurane during propofol anesthesia. CONCLUSION: Propofol suppressed the rCMRg of neocortex area more than sevoflurane, and sevoflurane suppressed the rCMRg of paleocortex, telencephalon more than propofol when the unconsciousness level was achieved by anesthesia. Sevoflurane produces different effects on relative brain glucose metabolism with propofol.
Anesthesia* ; Basal Ganglia ; Brain ; Electrons* ; Glucose* ; Healthy Volunteers ; Humans* ; Mesencephalon ; Metabolism* ; Neocortex ; Pons ; Positron-Emission Tomography* ; Propofol* ; Rabeprazole ; Telencephalon ; Thalamus ; Unconsciousness ; Visual Cortex ; Volunteers

OBJECTIVETo analyze the effects of aging or advanced glycation on gene expression in the cerebrum and spleen of female C57BL/6J mice.

METHODSThe gene expression profile was determined by using cDNA expression arrays containing 588 cDNA.

RESULTSAging and advanced glycation resulted in differential gene expression patterns of cerebrum and spleen compared with young mice. Among the 80 genes detected in cerebrum, 43 exhibited a change in mRNA ratios with aging or treatment. Thirty-four changes (79%) were common in aged and D-galactose treated mice, whereas the cerebrum from aged and AGE-lysine treated mice showed common changes in expression of 38 genes (88%). Of the 86 genes detected in spleen, 29 (34%) displayed an age-related decrease in expression, whereas 3 (3%) displayed an increase in expression levels with aging. Eighteen genes from the detectable genes exhibited expression changes in both cerebrum and spleen of mice.

CONCLUSIONSThe gene expression profiles of D-galactose and AGE-lysine treated mice resemble those of aged mice. Use of cDNA hybridization arrays may provide a promising tool to explore the mechanism of aging at a molecular level.

Aging ; physiology ; Animals ; Female ; Gene Expression Regulation ; Glucose ; metabolism ; Mice ; Mice, Inbred C57BL ; Oligonucleotide Array Sequence Analysis ; Spleen ; physiology ; Telencephalon ; physiology