Glia

Malignant and normal astrocytes can be induced to produce iNOS and NO. LPS alone stimulates astrocytoma cells but does not stimulate normal fetal astrocytes to make NO. IL-ljS is the best inducer of NO in both types 

TABLE I Total Nitric Oxide (Micromolar) Production by Human Adult Blood Macrophages, Fetal Microglia, and Fetal Mixed Glial Cells 

Treatment Macrophages Microglia Mixed glial cells  

While neonatal rat microglia produce NO in response to LPS or IFN-y within 24 hr after stimulation, recent data indicate that cytokine and/or LPS stimulation of purified human fetal microglia does not lead to NO production (Lee et al., 1993a) (Table I). However, as suggested earlier for human M ), the conditions under which NO is induced or even detected (e.g., does NO get scavenged before it can leave the cell ) require more work. 

A variety of human cells produce NO, but some cell types produce much more than others. In many cases the amount of NO produced by human blood M( ) is less than that produced by human glia. Both in the stimuli successfully used to induce NO and in the amount of NO produced, human glial cells and M( ) differ from these same cell types in the rodent. NO production by human blood Mc ) and glia is a more protracted process than it is in rodent cells, with the peak NO production taking 6-7 days in vitro. 

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In the most common method for chemiluminescent immunoassay (GLIA), after the immunological reaction and any necessary separation steps, the labeled compounds or complexes react with an oxidizer, eg, hydrogen peroxide, and an enzyme, eg, peroxidase, or a chelating agent such as hemin or metal... 

Adenosine is produced by many tissues, mainly as a byproduct of ATP breakdown. It is released from neurons, glia and other cells, possibly through the operation of the membrane transport system. Its rate of production varies with the functional state of the tissue and it may play a role as an autocrine or paracrine mediator (e.g. controlling blood flow). The uptake of adenosine is blocked by dipyridamole, which has vasodilatory effects. The effects of adenosine are mediated by a group of G protein-coupled receptors (the Gi/o-coupled Ai- and A3 receptors, and the Gs-coupled A2a-/A2B receptors). Ai receptors can mediate vasoconstriction, block of cardiac atrioventricular conduction and reduction of force of contraction, bronchoconstriction, and inhibition of neurotransmitter release. A2 receptors mediate vasodilatation and are involved in the stimulation of nociceptive afferent neurons. A3 receptors mediate the release of mediators from mast cells. Methylxanthines (e.g. caffeine) function as antagonists of Ai and A2 receptors. Adenosine itself is used to terminate supraventricular tachycardia by intravenous bolus injection. 

Induced by bacterial lipopolysaccharides or immune cytokines in macrophages, smooth muscle cells, and glia cells. Ca2+ is not required for the enzyme activation. 

Glycine transporter GlyTl (SLC6A9) CNS-glia -20 Clearance of interstitial neurotransmitter Sarcosine... 

The synthesis and metabolism of trace amines and monoamine neurotransmitters largely overlap [1]. The trace amines PEA, TYR and TRP are synthesized in neurons by decarboxylation of precursor amino acids through the enzyme aromatic amino acid decarboxylase (AADC). OCT is derived from TYR. by involvement of the enzyme dopamine (3-hydroxylase (Fig. 1 DBH). The catabolism of trace amines occurs in both glia and neurons and is predominantly mediated by monoamine oxidases (MAO-A and -B). While TYR., TRP and OCT show approximately equal affinities toward MAO-A and MAO-B, PEA serves as preferred substrate for MAO-B. The metabolites phenylacetic acid (PEA), hydroxyphenylacetic acid (TYR.), hydroxymandelic acid (OCT), and indole-3-acetic (TRP) are believed to be pharmacologically inactive. 

Simpson JE, Newcombe J, Cuzner ML, Woodroofe MN (1998) Expression of monocyte chemoattractant protein-1 and other beta-chemokines by resident glia and inflammatory cells in multiple sclerosis lesions. J Neuroimmunol 84 238-249 Simpson J, Rezaie P, Newcombe J, Cuzner ML, Male D, Woodroofe MN (2000) Expression of the beta-chemokine receptors CCR2, CCR3 and CCR5 in multiple sclerosis central nervous system tissue. J Neuroimmunol 108 192-200... 

Dziembowska M, Tham TN, Lau P, Vitry S, Lazarini F, Dubois-Dalcq M (2005) A role for CXCR4 signaling in survival and migration of neural and oligodendrocyte precursors. Glia 50 258-269... 

HIV-infected glia secrete inflammatory factors that can indirectly contribute to excitotoxicity (Giulian et al. 1996). The HIV envelope protein induces the secretion... 

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