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      Effect of Spleen-Cell-Conditioned Medium on [ 3H]-Choline Uptake by Retinal Cells in vitro Is Mediated by IL-2

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          Cytokines are essential molecules throughout the development of the nervous system and also play an important role during the adult life span. In the present work, we analyzed in vitro the effect of spleen-cell-conditioned medium (SCM) on the survival and [<sup>3</sup>H]-choline uptake of neonatal rat retinal cells. SCM induced an increase in neuronal survival, glial cell proliferation and neurite outgrowth, as evaluated by biochemical and morphological criteria. These effects were time dependent; after 120 h, SCM induced a 6-fold increase in the total protein level. The effect of SCM was blocked both by the inhibition of protein tyrosine kinase activity (10 μ M genistein) and by the inhibition of cell division (20 μ M fluorodeoxyuridine). SCM also increased the uptake of [<sup>3</sup>H]-choline by retinal cells. The effect was time dependent. The maximum effect was obtained after 48 h and was maintained at a high level until 120 h. Treatment by 10 μ M genistein and 15 μ M bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA-AM) (an intracellular calcium chelator) completely blocked this effect. However, 20 μ M fluorodeoxyuridine did not abolish it. Conditioned medium obtained from glial cells stimulated with SCM (S-GCM) induced an effect on [<sup>3</sup>H]-choline uptake earlier than that promoted by SCM. Anti-interleukin-2 (IL-2) antibodies blocked the effect of both SCM and S-GCM on [<sup>3</sup>H]-choline uptake after 48 and 72 h. IL-2 (50 U/ml) elicited the same effect as that observed when the cells were maintained in the presence of SCM. Taken together, our results suggest that IL-2 plays an important role in controlling the survival and differentiation of retinal cells in vitro.

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          Most cited references 5

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          Suppression of programmed neuronal death by sustained elevation of cytoplasmic calcium.

          Chronic depolarization greatly increases the survival of many types of neurons in culture. In at least some cases this enhancement of survival consists of the suppression of programmed cell death, a type of death occurring in developing neurons deprived of sufficient neurotrophic factor support. Available evidence suggests that the effect of depolarization on survival is mediated by a sustained rise of cytoplasmic free Ca2+, apparently caused by influx of Ca2+ through voltage-gated channels. This review discusses what is known about the mechanism by which prolonged depolarization and increased intracellular Ca2+ promote survival.
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            Interleukin-2 as a neuroregulatory cytokine

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              Cholinergic and acetylcholinesterase-containing neurons of the chicken retina.

              In the chicken retina, choline acetyltransferase-like immunoreactivity (ChAT-LI) defines three populations of cholinergic amacrine cells and two terminal bands in the inner plexiform layer (IPL). Acetylcholinesterase (AChE) histochemistry defines two prominent bands within the IPL which corresponded to those containing ChAT. Other AChE-positive bands in the IPL are not associated with cholinergic transmission sites. Cholinergic cell bodies contain AChE, but the most intensely AChE-positive cells do not appear to be cholinergic. AChE histochemistry may be used to define the major cholinergic synaptic sites in the IPL, and may be a useful marker of IPL lamination.

                Author and article information

                S. Karger AG
                May 2000
                04 May 2000
                : 7
                : 4
                : 195-207
                aDepartamento de Neurobiologia, Instituto de Biologia, Centro de Estudos Gerais, Universidade Federal Fluminense, Niterói, and bInstituto de Biofísica Carlos Chagas Filho, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil
                26439 Neuroimmunomodulation 2000;7:195–207
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 7, Tables: 4, References: 38, Pages: 13
                Original Paper


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