KEGG(Kyoto Encyclopedia of Genes and Genomes)〔和文〕 (特集 ゲノム医学の現在と未来--基礎と臨床) -- (データベース)

Introduction to synaptic circuits, Gordon M.Shepherd and Christof Koch membrane properties and neurotransmitter actions, David A.McCormick peripheral ganglia, Paul R.Adams and Christof Koch spinal cord - ventral horn, Robert E.Burke olfactory bulb, Gordon M.Shepherd, and Charles A.Greer retina, Peter Sterling cerebellum, Rodolfo R.Llinas and Kerry D.Walton thalamus, S.Murray Sherman and Christof Koch basal ganglia, Charles J.Wilson olfactory cortex, Lewis B.Haberly hippocampus, Thomas H.Brown and Anthony M.Zador neocortex, Rodney J.Douglas and Kevan A.C.Martin Gordon M.Shepherd. Appendix: Dendretic electrotonus and synaptic integration.

The synaptic organization of the brain

Chronic hepatitis C virus (HCV) infection occurs in about 3 percent of the world's population and is a major cause of liver disease. HCV infection is also associated with cryoglobulinemia, a B lymphocyte proliferative disorder. Virus tropism is controversial, and the mechanisms of cell entry remain unknown. The HCV envelope protein E2 binds human CD81, a tetraspanin expressed on various cell types including hepatocytes and B lymphocytes. Binding of E2 was mapped to the major extracellular loop of CD81. Recombinant molecules containing this loop bound HCV and antibodies that neutralize HCV infection in vivo inhibited virus binding to CD81 in vitro.

https://science.sciencemag.org/content/sci/282/5390/938.full.pdf

Binding of Hepatitis C Virus to CD81

Degeneration and regeneration of the nervous system

Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the p...

/pdf/biology-of-oligodendrocyte-and-myelin-in-the-mammalian-3ggbjcby4w.pdf

Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System

The neuronal response to injury as visualized by immunostaining of class III β-tubulin in the rat

A new application of the retrograde transport method designed to demonstrate neurons that project to two cortical areas has been developed. This method depends on the retrograde axonal transport of two markers, each of which is uniquely detectable by histological methods. In this study, horseradish peroxidase (detectable by the enzymatic reation product only) and tritiated proteins (either enzymatically inactive tritiated horseradish peroxidase or tritiated bovine serium albumin, both of which are detectable by the tritium label only) were used. One of these markers was injected into cortical area 17 and the other was injected into area 18.



In layers A and A1 of the lateral geniculate nucleus, 10% of the cells project to both area 17 and area 18 by axons that branch, 70% of the neurons project to area 17 only, less than 1% of the neurons project to area 18 only, and approximately 20% of the cells are probably interneurons. In the C laminae 50% of the cells project to both areas 17 and 18 by axons that branch, approximately 20% of the neurons project to area 17 only, 10% of the cells project to area 18 only, and about 20% of the neurons are unlabeled. The cells in the medial interlaminar nucleus project to area 17 only, to area 18 only, or to both of these areas by axons that branch.



In addition the retrograde markers were injected into single cortical areas, either area 17, area 18, or area 19. The injections of area 17 and those of area 18 confirmed the results of the double-label experiments, with 80% of the cells in the A laminae projecting to area 17 and approximately 10% projecting to area 18. Following injections of area 19, labeled neurons were seen in the medial interlaminar nucleus and the C laminae. Therefore, the medial interlaminar nucleus contains cells that project to areas 17, 18, and 19, with some cells projecting to both area 17 and area 18 by axons that branch. In the C laminae the analysis of the projection pattern could be carried further, for it was possible to determine the percentage of labeled neurons in this region. Since 80% of the cells project to areas 17 and 18, and since 60% of the cells of the C laminae were labeled following injections of area 19, many of the cells which project to area 19 must also project to either area 17 or area 18, and some cells must project to all three (areas 17, 18, and 19) by branching axons.

Cortical projections of the lateral geniculate nucleus in the cat.

In response to local injury, the retina presents a characteristic series of changes at the site of injury. A secondary series of changes then spreads to involve the entire retina, often resulting in progressive degenerative changes and the formation of scar tissue.1–6 These responses of the retina to injury can be divided into an early acute phase, a delayed subacute phase, and a late chronic phase.1,4,6

The early phase, which occurs within the first few hours after injury, is characterized by hemorrhage,1,3,5 alterations in the glutamatergic system,7 changes in ionic balance,8 and the beginning of cell-death cascades.9,10 It is during this early phase that the first changes in the transcriptome occur, with upregulation of the immediate early genes.9,10 The retina then undergoes a series of delayed cellular responses that last for days. Among these responses is a generalized inflammatory reaction in which damaged cells release proinflammatory cytokines that recruit peripheral blood components.1,3,6 Many retinal cells experience cell-type-specific responses: dedifferentiation, degeneration, migration, hypertrophy, and proliferation.4,9,11–13 For example, Muller glial cells and the retinal pigmented epithelium (RPE) enter a reactive state in which they change protein expression, proliferate, and migrate into the wound and vitreous space.4,6,11,12 Inflammation and cell proliferation resolve within the first week as the response to injury enters its chronic phase.1,4,6 During the late phase, RPE and Muller cells remain reactive and participate in structural remodeling of the retina. Cells that migrate into the wound and vitreous space replace the hemorrhage with fibrocellular membranes.1,4,6,12 With time, these membranes may contract, causing significant problems, including retinal detachment.1,4,6,12

Progress in understanding the mechanisms controlling secondary injury has been significant. Gains have come about by focusing on individual molecules5,14–16 or groups of molecules7–9,17 and their participation in specific processes of the retinal healing response. However, many of the molecular events associated with activation of this response remain unknown. In the present study, we used microarray technology to catalog the expression of thousands of genes after retinal injury. Our first approach was discovery-driven, using the power of microarray to define the global patterns of gene expression changes. The second approach was hypothesis-driven, focusing on the role of Cd81 (whose product is involved in proliferation and gliosis15,16,18–20) and markers of reactive gliosis, including the cytoskeletal protein glial fibrillary acidic protein (GFAP).1,5,11,14,21,22

/pdf/temporal-changes-in-gene-expression-after-injury-in-the-rat-2cf7by83nd.pdf

Temporal changes in gene expression after injury in the rat retina

The retinal afferents to the medial interlaminar nucleus and to its rostro-dorsal extension at the edge of the pulvinar have been studied in cats by fiber degeneration and autoradiographic methods. Fiber degeneration following section of one optic nerve shows two distinct retinal inputs: One is coarse-fibered and goes to the medial interlaminar nucleus itself; the second, which is fine-fibered, goes to the rostral and medial borders of the medial interlaminar nucleus and continues into the pulvinar. The regions in receipt of these fine fibers have been called the “geniculate wing”.



The topography of retinal representations and the degree of binocular overlap within the medial interlaminar nucleus and the wing have been studied by combining intraocular injections of 3H proline with local lesions of the injected eye, or with removal of the non-injected eye. In the medial interlaminar nucleus three distinct laminae are recognizable and are particularly clearly shown in horizontal sections. Rostrally and medially, lamina 1 maps the contralateral nasal retina as a mirror reversal of lamina A. Posterior and lateral to this, lamina 2 maps the ipsilateral temporal retina as a mirror reversal of lamina A1. Lamina 3 lies closest to the optic tract and receives crossed afferents from the temporal retina. In this lamina, which is the smallest, vertical retinal dimensions map as in the other layers, but we were unable to determine the mapping of the horizontal dimensions.



In the geniculate wing, as in the other geniculate layers, vertical lines of the visual field are mapped as corresponding vertical diencephalic dimensions; horizontal retinal dimensions are mapped as horizontal lines in the wing, with central retinal areas represented furthest from the optic tract. In the geniculate wing the contralateral nasal and ipsilateral temporal retina are mapped with considerable binocular overlap. The crossed temporal retina has no demonstrable representation in the wing.

Eldon E. Geisert

Papers

The neuronal response to injury as visualized by immunostaining of class III β-tubulin in the rat

Cortical projections of the lateral geniculate nucleus in the cat.

Temporal changes in gene expression after injury in the rat retina

An analysis of the retinal afferents to the cat's medial interlaminar nucleus and to its rostral thalamic extension, the “geniculate wing”

A mouse model of ocular blast injury that induces closed globe anterior and posterior pole damage.