Neuronal activity-induced Gadd45b promotes epigenetic DNA demethylation and adult neurogenesis.

The mammalian brain exhibits diverse types of neural plasticity, including activity-dependent neurogenesis in the adult hippocampus. How transient activation of mature neurons leads to long-lasting modulation of adult neurogenesis is unknown. Here we identify Gadd45b as a neural activity-induced immediate early gene in mature hippocampal neurons.

Reactive changes of retinal astrocytes and Müller glial cells in kainate-induced neuroexcitotoxicity.

The aim of this study was to investigate reactive changes of astrocytes and Müller glial cells in rats subjected to kainate treatment, which leads to neuronal degeneration in the ganglion cell layer and the inner border of the inner nuclear layer as confirmed by labelling with Fluoro-Jade B, a marker for degenerating neurons and fibres. Both the astrocytes and the Müller glial cells reacted vigorously to kainate injection as shown by their up-regulated expression of nestin, glial fibrillary acidic protein and glutamine synthetase. A major finding was the induced expression of nestin together with glial fibrillary acidic protein beginning at 1 day post-injection of kainate.

Microglia/macrophages responses to kainate-induced injury in the rat retina.

The present study was aimed to elucidate how retinal microglia/macrophages would respond to neuronal death after intravitreal kainate injection. An increased expression of the complement receptor type 3 (CR3) and an induction of the major histocompatibility complex (MHC) class II and ED-1 antigens were mainly observed in the inner retina after kainate injection. Prominent cell death revealed by Fluoro Jade B (FJB) staining and ultrastructural examination appeared at the inner border of the inner nuclear layer (INL) at 1 day post-injection.

Responses of microglia in vitro to the gram-positive bacterial component, lipoteichoic acid.

An increase in incidence and severity of gram-positive infections has emerged in the past decade. In this regard, attention has been focused recently on immune responses of microglial cells in the central nervous system to gram-positive bacteria. The underlying immunological and cellular events in microglial activation induced by specific bacterial toxin of gram-positive bacteria, however, have not yet been clarified fully.

Reactive changes of interstitial glia and pinealocytes in the rat pineal gland challenged with cell wall components from gram-positive and -negative bacteria.

Lipopolysaccharide (LPS), the major proinflammatory component of gram-negative bacteria, is well known to induce sepsis and microglial activation in the CNS. On the contrary, the effect of products from gram-positive bacteria especially in areas devoid of blood-brain barrier remains to be explored. In the present study, a panel of antibodies, namely, OX-6, OX-42 and ED-1 was used to study the response of microglia/macrophages in the pineal gland of rats given an intravenous LPS or lipoteichoic acid (LTA).

Skin manifestations of Kikuchi-Fujimoto disease: case report and review.

Unlabelled: Kikuchi-Fujimoto disease (KFD) is a histiocytic necrotising lymphadenitis, which is a benign disease of unknown aetiology. Misdiagnosing KFD as lymphoma or systemic lupus erythematosus is not uncommon due to the similarity of clinical and histopathological features of these diseases. A 12-year-old female suffered from cervical lymphadenopathy, leukocytopenia, fever and especially skin rash.

Regional heterogeneity in immunoreactive macrophages/microglia in the rat pineal gland.

Using specific macrophage antibodies (OX-42, OX-6, ED-1 and ED-2), this study examined the distribution of macrophages/microglia in the pineal gland of adult rats. Except for ED-2, all antibodies labeled distinct subpopulations of macrophages/microglia in the gland; ED-2 labeling was hardly detectable. The quantitative study showed that the pineal macrophages/microglia (PMM) expressing complement type 3 receptors (OX-42) were more numerous than those expressing the major histocompatibility complex class II antigen (OX-6) or unknown cytoplasmic/lysosomal antigens (ED-1).