More on Glutamate and its role in CTF

In 1990 Dr. Karl Jansen of the Maudsley Hospital in London wrote the following:

“Near-death experiences (NDE's) can be reproduced by ketamine via blockade of receptors in the brain (the N-methyl-D-aspartate, NMDA receptors) for the neurotransmitter glutamate. Conditions which precipitate NDE's (hypoxia, ischaemia, hypoglycaemia, temporal lobe epilepsy etc.) have been shown to release a flood of glutamate, over activating NMDA receptors resulting in neuro ('excito') toxicity. Ketamine prevents this neurotoxicity. There are substances in the brain which bind to the same receptor site as ketamine. Conditions which trigger a glutamate flood may also trigger a flood of neuroprotective agents which bind to NMDA receptors to protect cells, leading to an altered state of consciousness like that produced by ketamine.”

Clearly Jansen considers that glutamate is responsible for the classic Near-Death Experience. In this quotation he also acknowledges that glutamate is also responsible for many elements of temporal lobe epilepsy (TLE). In order for my "Scale of Transcendence" ( "SOT"- soon to be introduced to an unsuspecting world with the release of my latest book) to be credible I have to show that autism, migraine, bi-polar disorder, TLE and schizophrenia are also glutamate-induced. I have recently come across some interesting support for SOT. Examples as follows:

Autism
"The largest search for autism genes to date, funded in part by the National Institutes of Health (NIH), has implicated components of the brain's glutamate chemical messenger system and a previously overlooked site on chromosome 11. Based on 1,168 families with at least two affected members, the genome scan adds to evidence that tiny, rare variations in genes may heighten risk for autism spectrum disorders (ASD).The study is the first to emerge from the Autism Genome Project (AGP) Consortium, a public-private collaboration involving more than 120 scientists and 50 institutions in l9 countries. Their report is published online in the February 18, 2007 issue of Nature Genetics." - Quoted from Physorg.com, February 2007.

Migraine
“Migraine pain-relay centers, including the trigeminal ganglion, trigeminal nucleus caudalis, and thalamus, contain glutamate-positive neurons, and glutamate activates the trigeminal nucleus caudalis. Glutamate is implicated in cortical spreading depression, trigeminovascular activation, and central sensitization. Glutamate receptor-subtype antagonists are effective in preclinical models of migraine, and in the clinic.“ - Quoted from PMID: 12858134 [PubMed - indexed for MEDLINE. June 2003]

Temporal Lobe Epilepsy
"Elevated levels of extracellular glutamate in hyperexcitable areas of the brain, up-regulation of glutamate receptors, and loss of the glutamate-metabolizing enzyme, glutamine synthetase (GS), have all been reported in patients with mesial temporal lobe epilepsy (MTLE). Moreover, it appears that glial cells, particularly the astrocyte, may play a key role in the glutamate overflow in MTLE. Proliferation of astrocytes is a hallmark of the epileptogenic focus in MTLE." - "Brain" - 2008 Apr;131(Pt 4):938-44. Epub 2008 Mar 1. Quoted from a paper by M Sillanpää and D Schmidt, Department of Public Health, University of Turku, Turku, Finland.

B-Polar Disorder
"Disturbances of gamma-aminobutyric acid interneurons in the cerebral cortex contribute to the pathophysiology of schizophrenia and bipolar disorder. The activity of these neurons is, in turn, modulated by glutamatergic inputs furnished by pyramidal neurons." From a paper 'Acute mania is accompanied by elevated glutamate/glutamine levels within the left dorsolateral prefrontal cortex' by Michael N, Erfurth A, Ohrmann P, Gossling M, Arolt V, Heindel W, Pfleiderer B. (Psychopharmacology (Berl). 2003 Apr 9).

Clearly glutamate is the linking factor between each element of the SOT. As such I argue that it is reasonable to conclude that it has to be of some significance that glutamate is also a major contributor to the classic NDE .... an experience that may await us all in the final moments of our life.

Obviously I am keen to hear from anybody who has an opionion on this, but any comments from neurologists with regard to this observation will be most welcome. Am I right to make such a link or am I wrong to draw such conclusions?