I have stated many times that I am not an expert. I just post wh...

I have stated many times that I am not an expert. I just post what I find. This has been a mind boggling journey for me. This is way over my head but I struggle to read and understand. Finding answers to why children are suffering from neuro-psychiatric side effects is worth the effort. I have made the following observations. 1. Some quinoline are known to be able to cross the blood brain barrier. 2. Molecules that ionize are known to be more likely to be able to cross cell membranes. So if montelukast ionizes as a result of change in blood pH to sufficient acid conditions that it ionizes, then it could be possible or maybe like that it does in fact cross the blood brain barrier. 3. We know that there are cysLT1 receptors in the brain. 4. We know that researchers believe that montelukast may bind at the arginine of the cysLT1 receptor. 5. We know that arginine contains four nitrogens. And montelukast contains one. 6. We don't know what happens to those nitrogens. 7. We do know what macrophages create nitric oxide as I posted. 8. We do know that if something cause excessive nitric oxide to build in the brain that there would be damage to the neurons. Some people may remember when I got stuck at the astrocytes, the cysLT1 receptors and glutamate. I keep looking for research reports that may shed more light on this. Titre du document / Document title Nitric oxide causes glutamate release from brain synaptosomes Auteur(s) / Author(s) MCNAUGHT K. S. P. (1) ; BROWN G. C. (1) ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s) (1) Department of Biochemistry, University of Cambridge, Cambridge, ROYAUME-UNI Résumé / Abstract We determined the ability of pathological levels of nitric oxide (NO) to cause glutamate release from isolated rat brain nerve terminals using a fluorometric assay. It was found that NO (0.7 and 2 μM) produced (4 and 10 nmol/mg of synaptosomal protein) Ca2+-independent glutamate release from synaptosomes (after 1 min of exposure). Spermine/NO complex (spermine NONOate; a slow NO donor) and potassium cyanide (an inhibitor of cytochrome oxidase) also caused Ca2+-independent glutamate release. Preincubation of synaptosomes with 5 μM 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (an inhibitor of soluble guanylyl cyclase) had no effect on NO-induced Ca2+-independent glutamate release. Ca2+-independent glutamate release produced by NO was greater in a low-oxygen medium. NO, spermine NONOate, and potassium cyanide inhibited synaptosomal respiration with a similar order of potency with respect to their ability to cause glutamate release. Because NO has been shown previously to inhibit reversibly cytochrome oxidase in competition with oxygen, our findings in this study suggest that NO (and cyanide) causes glutamate release following inhibition of mitochondrial respiration at the level of cytochrome oxidase. Thus, elevated NO production leading to mitochondrial dysfunction, glutamate release, and excitotoxicty may contribute to neuronal death in neurological diseases. Revue / Journal Title Journal of neurochemistry ISSN 0022-3042 CODEN JONRA9 Source / Source 1998, vol. 70, no4, pp. 1541-1546 (29 ref.) INIST-CNRS, Cote INIST : 4037, 35400007527188.0230