I am re-posting this from June. I believe that we have many reas...

I am so glad you are back,i was worried about you.I see the meeting for the FDA is set for dec 10- thru 11 heres hoping they give a dam.Glad you are here

I just pulled this off the University of Bristol's website:

Glutamate is the major excitatory neurotransmitter in central nervous system (CNS) and as such the glutamate receptors play a vital role in the mediation of excitatory synaptic transmission (see animation). This process is the means by which cells in the brain (neurons) communicate with each other. An electrical impulse in one cell causes an influx of calcium ions and the subsequent release of a chemical neurotransmitter (e.g. glutamate). The transmitter diffuses across a small gap between two cells (the synaptic cleft) and stimulates (or inhibits) the next cell in the chain by interacting with receptor proteins. The specialised structure that performs this vital function is the synapse and it is in the synapse that the ionotropic glutamate receptors are generally found.

The ionotropic receptors themselves are ligand gated ion channels, ie on binding glutamate that has been released from a companion cell, charged ions such as Na+ and Ca2+ pass through a channel in the centre of the receptor complex. This flow of ions results in a depolarisation of the plasma membrane and the generation of an electrical current that is propagated down the processes (dendrites and axons) of the neuron to the next in line.

also read this: http://www.ajnr.org/cgi/content/full/22/10/1813

Glutamate excitotoxicity is the final common pathway resulting in neuronal injury for many seemingly unrelated disorders, including ischemia, trauma, seizures, hypoglycemia, hypoxia, and even some neural degenerative disorders. Familiarity with this process is important for neuroradiologists because of its central position in many of the disorders encountered in daily practice. This area has been one of the most intensely investigated fields in the neurosciences over the past several decades, and the information generated from this work will clearly influence our basic understanding of many neurologic disorders.

http://nutritionalconcepts.blogspot.com/2007/08/excess-glutamate-contributes-to-ocd.html

According to a report in Time Magazine, a gene that appears to regulate the brain chemical glutamate, when overstimulated by receiving too much (glutamate) from external sources (i.e. diet), can create Obsessive Compulsive Disorder.

http://www.reversebrain.net/Domin17.htm

BAD DREAMS IN ADULTS AS POSSIBLE RESULTS OF GUTAMATE EXCESS AND REVERSE HALF-BRAIN DOMINANCE DURING THE SLEEP.Renato Cocchi, a neurologist and a medical psychologist.

The nightmares and the bad dreams are nearly surely two different phenomena. While the nightmares appear primarily in childhood, the bad dreams in adult age, in persons with stress and depression, and often with troubles of the half-brain dominance. The bad dreams, - as usually death, misfortunes, accidents -, rarely induce the awakening, but they too can easily be recalled.

I suggested that the occurrence of bad dreams depend on glutamate excess during the sleep by its reduced turnover, and on greater easiness of the not dominant half-brain to recall negative contents for the oneiric activity, perhaps because more stimulated during the sleep,

Key words: Nightmare, bad dreams, waking up, stress, depression, half brain dominance, GABAA, GAD, glutamate, excess, turnover.

http://www3.interscience.wiley.com/journal/106558816/abstract

Glutamate is an important regulator of dendrite development; however, during cerebral ischemia, massive glutamate release can lead to neurodegeneration and death.

Here's more:
Over the last few years, evidence suggests that glutamate plays a role in depression.47,48 Patients with depression, both during an acute episode and during remission, have elevated levels of glutamate in some brain regions
http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=1590

To clarify my first reply, and not cause undue worry, when I quoted that "Glutamate is an important regulator of dendrite development; however, during cerebral ischemia, massive glutamate release can lead to neurodegeneration and death." This refers to destruction of neurons - not death of the person. This article was not about Singulair and the massive glutamate release discussed would be from lack of oxygen to the brain.

I know we are all concerned about long term or permanent damage to our children. As I have watched my own child recover, I do wonder what the future will bring and would like to see research conducted to address this issue.

I too believe that it crosses the blood brain barrier and the reason is that my son was given the adult 10ml size in a sample pack and the doc said to get a pill cutter and cut in half and give him 5ml each day. The pill is coated and I feel by cutting it in half it went right to the brain. He had side effects and horrific ones almost immediatley. I am sorry to say that he was only on the med for one week and has been off for 7 and still has anxiety. The nightmares are gone, hyperventalation is gone, wierd breathing pattern is mostly gone, leg aches are gone, open mouth tic is gone, panic attacks under control. It is so hard to believe that all this happened to him after one week and he is still having side effects. It has been a test of all our strength to get through this and I have only started being able to talk about it.

I don't understand the science behind this however, as a mother, I'm certain that this drug caused these side effects. In addition, I don't know if I'm paranoid or intiuitive but I felt that in the moment I told the immunologist this, he was fully aware of these side effects. Good luck with your research!