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Abstract  Glycogen represents the major brain energy reserve though its precise functions are still under debate. Glycogen has also been found in different cell types of the enteric nervous system (ENS), the largest and most complex component of the peripheral nervous system. In the present work we have demonstrated, by application of isozyme-specific antibodies, the presence of isozymes of glycogen phosphorylase (GP), one of the major control sites in glycogen metabolism, in the rat ENS. Immunohistochemistry revealed that isoform BB (brain) is the predominant isozyme expressed in enteric glial cells (EGC) and rare neurons of the myenteric and submucosal plexuses. Isoform MM (muscle) appears in cells which are, according to their location and morphology, probably interstitial cells of Cajal (ICC). In addition, both GP isoforms are expressed in longitudinal and circular intestinal smooth muscle layers. As GP BB is mainly regulated by the cellular AMP level, a special function of glycogen in the energy supply of neural gut functions is suggested. [ABSTRACT FROM AUTHOR]

Abstract Purpose  To investigate the membrane physiology of Müller glial cells from retinae of DBA/2J mice (which develop ocular hypertension) and of C57BL/6 control mice of different ages. Methods  Retinae were obtained at the ages of 3, 6, and 12 months from DBA/2J mice and from C57BL/6 controls. Immunohistochemistry was performed using antibodies against glial fibrillary acidic protein (GFAP). Whole-cell membrane currents, membrane potentials and capacitances were recorded from freshly isolated Müller cells. Results  Strong immunostaining for GFAP was found in Müller cells of 12-month-old DBA/2J mice, whereas only astrocytes were immunopositive in C57BL/6 retinae. No significant alterations of membrane currents or potentials of Müller cells from DBA/2J mice as compared to controls were observed at any age; however, the membrane capacitance was increased in Müller cells from DBA/2J mice at the age of 6 months. Conclusions  Although Müller cells of DBA/2J mice display some symptoms of reactive gliosis, the lack of significant alterations of the membrane physiology confirm previous data demonstrating that these cells undergo a nonproliferative gliosis. [ABSTRACT FROM AUTHOR]

Background Glial cells in human retinas and in fibrocellular membranes from patients with proliferative vitreoretinopathy (PVR) have been described to upregulate their expression of Y 1 receptors for neuropeptide Y (NPY) (Soler et al.: Glia 39:320, 2002). However, it is unknown whether Y 1 receptor activation causes proliferation of retinal glial cells. We investigated whether NPY exerts a proliferation-stimulating effect on retinal glial cells, and compared the NPY-evoked signaling with the signaling of purinergic P2Y receptors. Methods Proliferation assays using bromodeoxyuridine were carried out on primarily cultured Müller glial cells of the guinea pig, in the absence and presence of blockers of Y 1 receptors, of receptor tyrosine kinases (RTKs), of mitogen-activated protein kinases (MAPKs) and of phosphatidylinositol-3 kinase (PI3K). Results NPY exerted a biphasic effect on Müller cell proliferation. At low concentrations (0.1 ng/ml and 1 ng/ml) it decreased the proliferation rate of the cells, while at higher concentration (100 ng/ml) it increased Müller cell proliferation. The NPY-evoked proliferation was mediated by Y 1 receptor stimulation and by activation of the p44/p42 MAPKs and partially of the p38 MAPK. Moreover, Y 1 receptor-induced activation of PI3K as well as transactivations of the platelet-derived and the epidermal growth factor RTKs were necessary for full mitogenic effect of NPY. Y 1 and P2Y receptors share partially common signal transduction pathways in Müller cells. Conclusion It is suggested that NPY may be involved in stimulation of retinal glial cell proliferation during PVR when it is released at higher amounts into the injured retina. [ABSTRACT FROM AUTHOR]

Background. In chronic liver disease the neuroglial cells may be affected by neurotoxic metabolites which, in turn, could be expected to affect neuronal functions. The aim of this study was to evaluate the electroretinograms (ERG) from patients before and after liver transplantation, in order to study possible functional changes of the retina.Methods. Twelve patients with liver cirrhosis underwent routine ophthalmological examination and ERG before and after successful liver transplantation. Laboratory parameters, including ammonia, aspartate aminotransferase (AST), bilirubin, and cholinesterase, were compared. Patients were grouped according to the Child classification: three patients were Child A, six were Child B, three were Child C.Results. Most obvious ERG abnormalities were found in patients with cirrhosis Child C. Before transplantation 7 of 21 ERG parameters were out of the normal range, but in the follow-up examination after transplantation only one parameter was not within the normal range. Significant (P<0.05) postoperative improvements were found for the latencies of scotopic, mesopic and photopic b-waves and mesopic a-waves and for the photopic implicit time. Patients in the Child B group revealed less changes in the ERG. Before the transplantation only one parameter of the ERG was out of the normal range. All postoperative parameters were within the normal range. At 40±9 months after the liver transplantation a significant decrease in serum ammonia levels, AST and bilirubin and a significant increase in cholinesterase levels were observed.Conclusion. Patients with restored liver function after liver transplantation showed significantly improved ERG parameters. Our data suggest a recovery of the cells involved in hepatic retinopathy, including the Müller (glial) cells. [ABSTRACT FROM AUTHOR]