Ionic responses and growth stimulation in rat astroglial cells: Differential mechanisms of gangliosides and serum

Skaper, Stephen D.; Varon, Silvio

doi:10.1002/jcp.1041300320

Cited by 14 publications

(8 citation statements)

References 32 publications

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“…Soluble factors found in CM from cerebellar astrocytes decrease astrocyte proliferation (Aloisi et al, 1987), while an EGF receptor immunoreactive mitogen inhibitor has been reported in brain homogenate and astroglial CM (Nieto and Broderick, 1989). The presence of such an inhibitor may be undetectable in the current studies since 10% FBS is a strong mitogen to astrocytes (Skaper and Varon, 1987). Astrostatine, a soluble factor secreted by neurons (Rogister et al, 1990), has also been suggested as an inhibitor of astrocyte proliferation.…”

Section: Discussionmentioning

confidence: 96%

“…Mitogens and growth factors required for the continuous proliferation of astrocytes may drop below threshold levels during maturation, and as a consequence proliferating cells exit the cell cycle. In vitro studies suggest that among the major mitogens for astrocytes are epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and platelet-derived growth factor (PDGF; Besnard et al, 1987;Hunter et al, 1993;Skaper and Varon, 1987). These ligands drive robust proliferation of cultured astrocytes and are present in the developing and adult CNS.…”

Section: Introductionmentioning

confidence: 99%

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Homotypic cell contact-dependent inhibition of astrocyte proliferation

Nakatsuji

Miller

1998

Glia

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Homotypic cell contact-dependent inhibition of astrocyte proliferation

Nakatsuji

Miller

1998

Glia

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“…In this regard, bFGF may be paradigmatic. Basic FGF is a well-known stimulator of astrocyte and oligodendrocyte proliferation [196,197]. The mRNA level of bFGF has been shown to be reduced in the dorsolateral prefrontal cortex of patients with major depression [92,198].…”

mentioning

confidence: 99%

Gliogenesis and Glial Pathology in Depression

Rajkowska¹,

Miguel-Hidalgo²

2007

CNSNDDT

534

364

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Recent research has changed the perception of glia from being no more than silent supportive cells of neurons to being dynamic partners participating in brain metabolism and communication between neurons. This discovery of new glial functions coincides with growing evidence of the involvement of glia in the neuropathology of mood disorders. Unanticipated reductions in the density and number of glial cells are reported in fronto-limbic brain regions in major depression and bipolar illness. Moreover, age-dependent decreases in the density of glial fibrillary acidic protein (GFAP) -immunoreactive astrocytes and levels of GFAP protein are observed in the prefrontal cortex of younger depressed subjects. Since astrocytes participate in the uptake, metabolism and recycling of glutamate, we hypothesize that an astrocytic deficit may account for the alterations in glutamate/GABA neurotransmission in depression. Reductions in the density and ultrastructure of oligodendrocytes are also detected in the prefrontal cortex and amygdala in depression. Pathological changes in oligodendrocytes may be relevant to the disruption of white matter tracts in mood disorders reported by diffusion tensor imaging. Factors such as stress, excess of glucocorticoids, altered gene expression of neurotrophic factors and glial transporters, and changes in extracellular levels of neurotransmitters released by neurons may modify glial cell number and affect the neurophysiology of depression. Therefore, we will explore the role of these events in the possible alteration of glial number and activity, and the capacity of glia as a promising new target for therapeutic medications. Finally, we will consider the temporal relationship between glial and neuronal cell pathology in depression.Glial cells were first identified as non-neuronal elements in the nineteenth century by the anatomist R. Virchow (after [1]). At that time glia were thought to be no more than silent supportive "glue" for neurons and that glia were unable to participate in information processing. In the past two decades, research has changed this perception and provided evidence for glia being important dynamic partners of neuronal cells actively participating in brain metabolism, synaptic neurotransmission and communication between neurons [2]. The discovery of new glial functions coincides with growing evidence for the involvement of glia in the neuropathology of neurological [3] and more recently, psychiatric disorders, such as major depression and manic-depressive (bipolar) illness (reviewed in [4]) TYPES OF GLIAL CELLSGlia are the most numerous cells in the human brain, outnumbering neurons by a ratio of ten to one [5] (Fig. 1). This ratio drops to one-to-one in rodents [5,6] implying that increases in glia over neurons are associated with the progressive development of higher brain functions [7]. Although anecdotal, it is interesting that in the brain of Albert Einstein, the neuron/glia ratio in the associational parieto-temporal cortical area 39 was found to be smaller ...

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“…Radiolabeling of trichloroacetic acid-insoluble material was determined as described previously [37]. The final pellet was resuspended in RPMI 1640 plus 10 per cent FCS and diluted to a concentration of 5000 cells/ml.…”

Section: Cell Growth In Vitromentioning

confidence: 99%

Exogenously administered gangliosides fail to increase in vivo metastatic frequency or in vitro growth of murine neoplastic cells

et al. 1990

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The influence of gangliosides on tumor growth and frequency of metastasis in vivo, as well as growth of neoplastic cells in vitro, was tested utilizing the mouse fibrosarcoma cell line MN4. In mice receiving intramuscular tumor transplants, injections of a ganglioside mixture twice daily did not influence the tumor volume or the number of spontaneous metastases per animal. Furthermore, in mice receiving the cells by tail vein injection, injections of a ganglioside mixture once or twice daily did not affect the number of metastatic foci in the lungs. Preincubation of neoplastic cells with the ganglioside mixture decreased the number of metastatic foci in the lungs of mice receiving the cells by tail i.v. injection. The addition of ganglioside mixture to the culture medium for up to a 48-h incubation period had no effect, independently of the cell density utilized, on either the rate of DNA synthesis or the relative numbers of neoplastic cells as compared to controls; at higher ganglioside concentrations, growth was actually reduced. These results are interpreted to indicate that gangliosides, under the present conditions, do not influence tumor growth and metastatic neoplastic capacity in vivo, and growth in vitro.

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Ionic responses and growth stimulation in rat astroglial cells: Differential mechanisms of gangliosides and serum

Cited by 14 publications

References 32 publications

Homotypic cell contact-dependent inhibition of astrocyte proliferation

Homotypic cell contact-dependent inhibition of astrocyte proliferation

Gliogenesis and Glial Pathology in Depression

Exogenously administered gangliosides fail to increase in vivo metastatic frequency or in vitro growth of murine neoplastic cells

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