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Schwann cells play an important role in peripheral myelination, and dysfunction of these cells leads to axonal damage. Schwann cells degenerate following peripheral nerve injury. Immature Schwann cells proliferate, differentiate, and support axonal regeneration and extension during recovery. There are a lot of intracellular signals involved in the myelination process. Although serum- and glucocorticoid-inducible kinase (SGK

The occipital transtentorial route is considered the most suitable for surgical treatment of lesions arising from the anterosuperior cerebellum, upper fourth ventricle, and upper dorsal brain stem. Therefore, this study examined the feasibility and effectiveness of the endoscopic high occipital interhemispheric transtentorial approach (EHOTA) for lesions in these areas, in achieving results comparable to the endoscopic occipital interhemispheric transtentorial approach (EOTA). EOTA has recently been reported to be an effective procedure for pineal region tumors, having several advantages that include minimal invasiveness with a small entrance limiting the retraction of the occipital lobe, the elimination of blind spots, and the facilitation of fine manipulation due to the bright, magnified panoramic view.By using 30 clinical datasets of venous-phase head computed tomography angiogram, measurements on images were performed and differences between EOTA and EHOTA were identified. In addition, the feasibility of EHOTA was verified with 5 cadaver heads.Although the operative field via EHOTA was considered significantly deeper and less maneuverable than with the procedure via EOTA, beneficial angles for manipulation in the superior cerebellum and the fourth ventricle were obtained in EHOTA, on account of their becoming more obtuse. Using EHOTA, it was possible to reach those regions and effectively manipulate all 10 sides of the 5 cadaveric heads, as well as a case with anterosuperior cerebellar cavernous angioma.EHOTA, which has the same advantages as EOTA, could prove to be an efficacious procedure for lesions in the anterosuperior cerebellum, upper fourth ventricle, and upper dorsal brain stem.

Background Profound changes in gene expression can result from abnormalities in the concentrations of sequence-specific transcription factors like specificity protein 1 ( Sp1 ). Specificity protein 1 binding sites have been reported in the promoter regions of several genes implicated in autism. We hypothesize that dysfunction of Sp1 could affect the expression of multiple autism candidate genes, contributing to the heterogeneity of autism. Methods We assessed any alterations in the expression of Sp1 and that of autism candidate genes in the postmortem brain (anterior cingulate gyrus [ACG], motor cortex, and thalamus) of autism patients ( n = 8) compared with healthy control subjects ( n = 13). Alterations in the expression of candidate genes upon Sp1 /DNA binding inhibition with mithramycin and Sp1 silencing by RNAi were studied in SK-N-SH neuronal cells. Results We observed elevated expression of Sp1 in ACG of autism patients ( p = .010). We also observed altered expression of several autism candidate genes. GABRB3 , RELN , and HTR2A showed reduced expression, whereas CD38 , ITGB3 , MAOA , MECP2 , OXTR, and PTEN showed elevated expression in autism. In SK-N-SH cells, OXTR , PTEN , and RELN showed reduced expression upon Sp1 /DNA binding inhibition and Sp1 silencing. The RNA integrity number was not available for any of the samples. Conclusions Transcription factor Sp1 is dysfunctional in the ACG of autistic brain. Consequently, the expression of potential autism candidate genes regulated by Sp1 , especially OXTR and PTEN , could be affected. The diverse downstream pathways mediated by the Sp1 -regulated genes, along with the environmental and intracellular signal-related regulation of Sp1 , could explain the complex phenotypes associated with autism.

Olfactory receptors are G-protein coupled receptors and are encoded by an extremely large and diverse family of genes in mammals. There is increasing evidence that olfactory receptors are widely distributed in many organs, suggesting that olfactory receptors do not only recognize airborne odorants but also play important roles in chemotaxis or organ construction in embryo. In this study, we investigated whether olfactory receptors and their transduction molecule, Golf are expressed in the rat placenta. By RT-PCR, we identified 11 different olfactory receptor genes, which are all members of class II, in the rat placenta cDNAs, and our results suggested that particular members of the olfactory receptor gene family might be preferentially expressed in the placenta. By western blot analysis, we demonstrated that Golf protein is expressed in the placenta and its expression levels are developmentally regulated. We found that Golf immunoreactivity is exclusively localized to giant cell trophoblasts and spongiotrophoblast cells. These findings raised a possibility that a particular subset of olfactory receptors might be coupled with Golf and function in giant cell trophoblasts and spongiotrophoblast cells.

Astrocytic contribution of endothelial cell monolayer permeability was examined in two blood-brain barrier (BBB) models, using the coculture in a double chamber system: rat astrocytes and bovine aortic endothelial cells (BAECs) or bovine brain endothelial cells (BBECs). In system 1, where astrocytes were separated from endothelial cells, a 40% reduction in L-glucose permeability of the BBEC monolayer, but not the BAEC monolayer, was observed by cocultivation with astrocytes. Although several passages of BBEC in culture elicited morphological transformation from spindle-shapes to cobblestone-like features, the passaged BBECs remained responsive to astrocytes in coculture in system 1 (37% reduction of the L-glucose permeability). By contrast, in system 2, where respective endothelial cells and astrocytes layered on the upper and lower surfaces of a membrane, the permeability of both BAEC and BBEC monolayers was reduced by cocultivation with astrocytes (75% reduction for BAEC and 40% reduction for BBEC). BAECs in this contiguous coculture (system 2) with astrocytes showed numerous tight junction-like structures characteristic of the BBB in vivo. These results suggest that primary cultured BBECs, which had been primed by astrocytes in vivo, retain a higher sensitivity to astrocytes possibly through an astrocytic soluble factor (s) to exhibit BBB-specific phenotypes, and that even BAEC from extra-neural tissues, when cultured with astrocytes in close proximity in vitro, may acquire the similar phenotypes and serve for an extensive use of BBB model in vitro.

Glial contribution to in vitro synaptic function was investigated in a neuron-glia co-culture system by monitoring spontaneous oscillations of intracellular Ca 2+ in neurons. Rat cortical neurons, grown stably on a cortical astrocyte monolayer, extended neurites resulting in marked functional synapse formation. Little synapse formation was observed in neuronal co-culture with meaningeal fibroblasts or endothelial cells. Aged astrocytes in vitro (C35) were found to attenuate synaptic development, while young astrocytes (C5) markedly promoted synaptic function. C5 and C35 astrocyte media conditioned yielded no significant synaptogenic effect, indicating diffusible factor(s) are not responsible for our observation. Modulation of astrocytic proliferation and differentiation by gliostatin, a glial growth inhibitor, or dibutyryl cAMP affected neuronal synaptic function on the co-cultures. Site-specific analysis in homologous and heterologous neuron-astrocyte co-cultures among cortex, hippocampus, septum, and striatum revealed that homologous combinations of neurons and astrocytes derived from identical brain regions elicited the largest number of synchronizing neur`ons. Thee results suggest that in vivo neuronal synaptic function essentially requires the participation of adjacent astrocytes, which is site-specific and age-dependent.

Gliostatin is a polypeptide factor (apparentMr = 100k with a homodimeric structure comprising two 50 kDa subunits) acting on cortical neurons (neurotrophic action) as well as astrocytic cells (growth inhibition). Under the coculture system of cerebral cortical neurons and astrocytes from fetal rats (E15 or E16), the neurotrophic action of gliostatin was examined immunocytochemically. Immunostaining by an anti-neurofilament (NF) monoclonal antibody visualized a marked neurite-outgrowth and interconnecting bundles of neuritic processes induced by gliostatin in the coculture system. Neurons stimulated by gliostatin formed dense aggregates in clumps, while neurons in control coculture spread out. Gliostatin has also shown survival-promoting effects on neurons. Furthermore, it was shown that gliostatin induced the differentiation of protoplasmic astrocytes to fibrous astrocytes. These results further support our previous contention that gliostatin plays physiological roles on neuronal and glial development.