Ischemic damage in the selectively vulnerable populations of neurons is thought to be caused by an abnormal accumulation of intracellular calcium. It has been reported that the neurons, expressing specific calcium binding proteins, might effectively control intracellular calcium concentrations because of a high capacity to buffer intracellular calcium in the brain ischemic condition. It is uncertain that parvalbumin, one of the calcium binding proteins, can protect the neurons from the cerebral ischemic damage. Recently, treatment of kappa opioid agonists increased survival rate, improved neurological function, and decreased tissue damage under the cerebral ischemic condition. Many evidences indicate that these therapeutic effects might result from regulation of calcium concentration. This study was desighed to analyze the changes of number in parvalbumin-positive neurons after cerebral ischemic damage according to timepoints agter cerebral ischemic inductionl In addition, we evaluated the effect of GR89696 (kappa opioid agonist) or naltrexone(non selective opioid antagonist) on the changes of number in parvalbumin expressing neurons under ischemic condition. Cerebral ischemia was induced by occluding the common carotid artery of experimental animals. The hippocampal areas were morphometrically analyzed at different time point after ischemic induction(1, 3, 5 days) by using immuno-histochemical technique and imaging analysis system. The number of parvalbumin-positive neurons in hippocampus was sighificantly reduced at 1 day after ischemia(p0.05). Furthermore, the number of parvalbumin-immunoreactive neurons was dramatically reduced at 3 and 5 days after cerebral ischemic induction(p0.05) as compared to 1 day group after ischemia, as well as sham control group. Sighificant reduction of parvalbumin positive neurons in CA1 region of hippocampus was observed at 1 day after cerebral ischemic induction. However, sighificant loss of MAP2 immunoreactivity was observed at 3 day after cerebral ischemia. The loss of parvalbumin-positive neurons and MAP2 immunoreactivity in CA1 region was prevented by pre-administration of GR89696 compared to that of saline-treated ischemic group. Furthermore, protective effect of GR89696 partially reversed by pre[treatment of naltrexone. These data indicate that parvalbumin-positive neurons more sensitively responded to cerebral ischemic damage than MAP2 protein. Moreover, this loss of parvalbumin-positive neurons was effectively prevented by the pretreatment of kappa opioid agonist. It was also suggested that the changes of number in parvalbumin-positive neurons could be used as the specific marker to analyze the degree of ischemic neuronal damage.

A 13-year-old female Miniature Pincher was euthanized after suffering from respiratory insufficiency and seizure. At necropsy, firm tan masses approximately 4 to 5 cm in diameter were noted at the right caudal lobe and left cranial lobe of the lung. On cross sections of the cerebellum and the cerebrum, several compressive firm round masses, 0.5 to 1 cm in diameter, were noted. Similar looking nodules were also present in the mediastinal lymph nodes. Histopathologically, the neoplastic masses consisted of cuboidal shape epithelial cells that form glandular structure.

To elucidate the involvement of interleukin-1beta converting enzyme (ICE) in the courseof experimental autoimmune encephalomyelitis (EAE), we induced EAE by immunizing rats with an emulsion of rat spinal cord homogenate with complete Freund's adjuvant supplemented with Mycobacterium tuberculosis(H37Ra, 5mg/ml) and then examined the expression of ICE in the spinal cord of rats with EAE. In normal rate spinal cords, ICE is constitutively, but weakly, expressed in ependmal cells, neurons, and some neuroglial cells. In EAE, many inflammatory cells are positive for ICE, and the majority of ICE+ cells were identified as ED1+ macrophages. During this stage of EAE, the number of ICE+ cells in brain cells, including neurons and astrocytes, increased and these cells also had incresed ICE immunoreactivity. These findings suggest that the upregulation of ICE in both brain cells and invading hematogenous cells is stimulated by a secretory product from inflammatory cells, and that this enzyme is involved in the pathogenesis of EAE via the production of IL-1 beta.

This study was undertaken to examine the developmental expression of osteopontin(OPN) in the mouse brain. In Western blotting analysis, the expression of OPN was noted initially at embryonic stage and increased gradually after birth and decreased at postnatal day 60(P60). In immunohistochemistry, OPN expression was found in the interstitial nucleus Cajal and the substantia nigra reticularis in anterior part of the brain and in the inferior olivary complex, the parabrachial nucleus, the facial nucleus, the gigantocellular reticular nucleus, the trigeminal nucleus and the anterior interposed nucleus in posterior part of the brain at P31 and P60.

In order to study about the lobule and layer formation and cell migration of the mouse cerebellum from at the birth to 15th day effected by 2.5, 5 and 10 Gy r-raddiation at the 19th pregnancy. The routine tissue preparation and staining procedure, Immunohistochemical staining method by the several antibody and western brotting method were utilized from the birth to the 15th day. The results were as followings. 1. The body and cerebellum weights were more slowly increase of the the 2.5 Gy, 5 Gy and 10 Gy irradiation group compare to the control group, and the health condition of the 2.5 Gy group was a little bad. but the 10 Gy group was more severe and begun to die from the 12th day after birth.

Galectin family, endogenous β-galactoside-binding animal lectins, is known for the role in cell differentiation, morphogenesis, apoptosis and tumorigenesis. Galectin-3, one of family member, has been studied for its role in cell differentiation and tumor metastasis, and for its expression on epithelial cells of colon and mast cells but not in brain. Several reports, however, suggest its expression in brain including as a prion binding protein. In this report we explored possibility of galectin-3 expression in brain tissue.