Cytoplasm Of Neuronal Cells Research Articles

Absence of anti-P/Q calcium channel antibody in the sera of patients with anti-Yo antibody-positive paraneoplastic cerebellar degeneration.

Subacute cerebellar ataxia in patients with cancer in whom metastasis to the cerebellum has not occurred and who exhibit neither infection, side effects of chemotherapy, nor nutritional deficiencies, is designated paraneoplastic cerebellar degeneration (PCD). A group of women with PCD and ovarian or uterine cancer harbor an anti-Yo antibody in their sera and CSF.1 Anti-Yo antibody binds to 52- to 62-kD and 34-kD proteins on Western blots of human Purkinje cell extracts and reacts with Purkinje and other neuronal cell cytoplasm on immunohistochemical analysis. This antibody may be produced against tumor antigens that also react with neuronal proteins. However, there is no evidence that anti-Yo antibody causes neuronal damage. We have failed in numerous attempts to produce animal models of PCD by injection of serum IgG from patients with PCD into rodent brains or by immunization of rodents with recombinant Yo protein; neuronal degeneration was not induced in any of these cases.2 However, the sera of PCD patients could contain minor antibodies …

Photoemission analysis of chemical differences between the membrane and cytoplasm of neuronal cells

We demonstrate the possibility of using x-ray photoemission spectroscopy (XPS) to distinguish between the chemical properties of the neuron membrane and of the cytoplasm in brain cells. This was possible by analysing cells de-capped by using a newly developed technique. The XPS spectra clearly show chemical differences between the cell cytoplasm and the membrane, for example between nitrogen in and , which are characteristic of the proteins and membrane phospholipids, respectively. A preliminary (and not conclusive) interpretation of all the observed spectroscopic features is given.

Pyridoxal kinase immunoreactivity in rabbit brain.

Murine polyclonal antibody against purified bovine brain pyridoxal kinase (EC 2.7.1.35) was generated and showed cross-reactivity with rabbit brain pyridoxal kinase. This antibody was used to immunohistochemically examine the distribution of pyridoxal kinase in the rabbit brain. The cytoplasm of neuronal cells and neuroglial cells in the cerebral cortex, hippocampal region, brain nuclei and cerebellar cortex showed positive staining with various degrees of intensity. The neuronal cells and surrounding fibers in some brain nuclei, such as the area tegmentalis ventralis or the substantia nigra, showed intense staining. The neuronal cells of the hippocampal region showed somewhat weak reactivity, but some with intense reactivity were found sparsely distributed and positive staining fiber networks of a very low density were also observed.

Immunohistochemical localization of gonadotropin-associated peptide (GAP) in the human hypothalamus.

GAP was immunohistochemically localized for the first time in the human hypothalamus. GAP-immunoreactivity was present in the cytoplasm of neuronal cells in the arcuate nucleus. GAP-immunoreactive nerve fibers were also present in the primary plexus around capillaries in the infundibular region. No GAP-immunoreactive neurons were detected in the paraventricular nuclei or supraoptic nuclei.

Localization of immunoreactive lipocortin-1 in the brain and pituitary gland of the rat. Effects of adrenalectomy, dexamethasone and colchicine treatment

The presence and localization of endogenous lipocortin-1 (LC-1, a protein which has been proposed to mediate the anti-inflammatory actions of the glucocorticoids) was studied by immunohistochemical techniques in rat brain and pituitary. A polyclonal antiserum specific for a fragment of lipocortin-1 (αα1–188) was used to visualize immunoreactive LC-1 (iLC-1) in both neuronal and non-neuronal cell structures. Neuronal staining, which was independent of microtubular axonal transport mechanisms (in that it was not affected by blockade of axonal transport), was found in varicose nerve fibres in various regions of the brain. In addition, iLC-1 was found in the cytoplasm of neuronal cells throughout the brain. Of all brain regions which showed iLC-1, only the hippocampal neurons showed a reduced staining intensity after adrenalectomy. However, iLC-1 was not affected by dexamethasone treatment. Non-neuronal iLC-1 was found in ependymocytes lining the cerebral ventricles and aqueduct. In addition, iLC-1 was found in tanycytes in all circumventricular organs studied and in the ventral walls of the third ventricle, where some of the branching tail processes appeard to envelop local capillaries and neuronal cell bodies.A tancycyte-mediated release of LC-1 from varicose nerve fibres into the portal vasculature is proposed.

若齢牛の大脳皮質壊死症

Eight young cattle with neurologic signs were encountered at the Hamamatsu City Meat Center in these five years. In them, the cerebral cortex was affected with widespread lamellar necrosis, which involved the whole cortex in some cattle. The cytoplasm of neuronal cells was eosinophilic and shrunk with pyknotic nuclei. These changes were probably due to ischemia of the cerebral cortex. In the surrounding tissue, there were numerous phagocytic cells with foamy cytoplasm containing lipids to result in cystic areas. Necrosis of neuronal cells was present in the cerebral nuclei, thalamus, substantia nigra, corpora quadrigemina and vermis cerebelli, as well as in the cerebral cortex.These necrotic changes of neuronal cells, the age of affected animals ranging from 5 to 12 months, and the sporadic occurrence suggested that the eight cases might be diagnosed as “cerebrocortical necrosis of cattle” or “polioencephalomalacia of cattle”, although neither etiology nor pathogenesis was completely investigated.