Glial cells source

Glucocorticoid. Adrenal steroid receptors have been subdivided into two categories, one of which is the classical glucocorticoid receptor [7,19]. This receptor, cloned from human and rat sources, consists of a steroid- and DNA-binding subunit of 95 kDa [7, 19]. Such receptors, which have dissociation constants of 4-5 nM for glucocorticoids, are widely distributed across brain regions and are found in neurons and glial cells [7,19]. 

Activated macrophages and microglia are likely cellular sources of IL-1 in the central nervous system. IL-la and p, both 17-kDa proteins, are the products of two distinct genes and produce many of the same effects that TNF has on glial cells. IL-1 upregulates cytokine production, includes cell surface molecules, activates nitric oxide, and stimulates proliferation. When used alone, IL-1 and TNFa both stimulate nitric oxide production in C6 cells. However, in human fetal astrocyte cultures, IL-1 is a better nitric oxide inducer when used in combination with IFNy. 

Glial cells are a source of multiple cytokines, including interleukin-1 /3 (IL-1 /3), IL-6, and tumor necrosis factor-a (Hanisch, 2002). These cytokines can contribute to different features of pathological pain, although their role within the spinal cord has not been completely understood (DeLeo and Yezierski, 2001 Watkins... 

Astrocytes. Astrocytes constitute about 85% of all glial cells in the CNS thus their numbers surpass all other cell types, including neurons. Occupying this large fraction of total neural mass, it is perhaps not surprising that astrocytes maintain connections with both microvasculature and neurons. This positioning puts them in immediate contact with the incoming source of most neurotoxicants, the blood. Consequently, part of the protective function of astrocytes is their critical role in the formation of the blood-brain barrier (further discussed in Section 31.4.2.2). Astrocyte endfeet (the widened ends of astrocyte projections) wrap around capillaries and encapsulate... 

Several ceU sources have been used for experimental ceU therapy approaches pluripotent stem cells like embryonic stem cells from the blastocyst and embryonic germ cells [47, 48], human cord-blood derived cells [49], but also cultured cell lines. Neural stem cells (stem cells forming neuronal as well as glial cell lineages) isolated from different parts of the brain known to harbor multipotent neural stem cells [50-52] are also an option. In a non-neurode-generative indication, a cultured cell line was used to treat patients after stroke in a pilot clinical trial. The cells were transplanted in the paramedian plane and treatment was reported to be safe, with signs of efficacy [53]. 

Hexokinase, which is in the cytoplasm of neurons and glial cells, is a key enzyme in the utilization of glucose as an energy source. After active transport of FDG into cells, hexokinase catalyzes the phosphorylation of glucose to glucose-6 phosphate. 

It appeared, furthermore, that synaptosomal plasma membranes (SPMs) could easily be obtained after lysis and ftuther subcellular fractionation of such synaptosomal preparations. Essentially, this procedure permits isolation of synaptosomal plasma membranes with minimal contamination by glial cell elements. Throughout the years, this method has been modified and improved in many labs to permit detailed studies of neuronal signal transduction using isolated synaptosomal plasma membranes in vitro. Recently, synaptosomal plasma membranes have been used to study protein phosphorylation and dephosphorylation events (6-9), polyphosphomositide metabolism (10), and protein-protein interactions using chemical crosslinkers (9,11) and unmuno-precipitation techniques (6,12). Synaptosomal plasma membranes have also been used as source material for isolation of membrane proteins (13). 

As noted earlier, glial cells are a potentially important component of the blood-brain barrier. In our laboratory, we are investigating the uptake of thyroid hormone into cultured cells as models of intracellular uptake in the CNS, and we have included a human glioma cell line in these studies. We have also made a point of looking at the uptake of T as well as T3 since the major source of intracellular T3 in nerve cells is from monodeiodination of T after it is taken into the cell. In the glioma cells as well as in human and mouse neuroblastoma cells and human medulloblastoma cells, specific transport of thyroid hormones can be demonstrated at the plasma membrane. Thus, nervous system cells share this property with hepatocytes, skeletal myoblasts and several other cell types that have been investigated ... 

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