Ema
Senior Member
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I started LDN because I thought it would help decrease levels of glutamate in my brain. It is widely reported that LDN inhibits glial cells which produce glutamate on LDN pages.
Like this one:
http://www.ldnresearchtrust.org/node/188
However, LDN increases levels of beta endorphins drastically...which have been shown to enhance glutamate neurotoxicity in the hypothalamus by disrupting the calcium balance.
http://www.ncbi.nlm.nih.gov/m/pubmed/11938958/?i=2&from=/10374630/related
How can both of these things be true? Any ideas?
Like this one:
Glutamate is the most abundant neurotransmitter found in the central nervous system. It is an excitatory neurotransmitter. Glutamate binds to a receptor called NMDA (N-methyl D-aspartate).
The NMDA receptor is the most common receptor found in the Central Nervous System. When the NMDA receptor is activated by glutamate it opens up calcium channels which cause the nerves to fire.
To summarize, when glial cells are activated they release chemicals and neurotransmitters that cause NMDA receptors to be activated which cause nerves to fire.
LDN (Low Dose Naltrexone), by its ability to inhibit microglial activation, suppresses activation of NMDA receptors by decreasing the release of glutamate neurotransmitter.
http://www.ldnresearchtrust.org/node/188
However, LDN increases levels of beta endorphins drastically...which have been shown to enhance glutamate neurotoxicity in the hypothalamus by disrupting the calcium balance.
The effects of beta-endorphin(beta-End) on monosodium glutamate(MSG) neurotoxicity were studied via morphological observation and image analysis of neuronal areas, together with the determination of intracellular free calcium concentration ([Ca2+]i) in single neuron and radioimmunoassay for beta-End contents.
beta-End(1.0 mg.kg-1, s.c.) was found to obviously aggravate the neuronal injury in the arcuate nucleus of hypothalamus induced by MSG(0.5 g.kg-1, s.c.).
Just as MSG increased [Ca2+]i significantly, beta-End(2.0 g.L-1) itself also increased it, though the extent of elevation was smaller than that of MSG(17.0 mg.L-1).
The obvious changes of [Ca2+]i induced by both MSG and beta-End were partially reversed after pretreatment with verapamil.
On the other hand, the content of beta-End in different areas of the brain were augmented following the addition of MSG and further elevated by morphine treatment.
These findings suggest that the mechanisms of the enhancing effect of beta-End on glutamate neurotoxicity were linked to the aggravation on the disruption of intracellular Ca2+ homeostasis induced by MSG. Moreover, the fact that opioids promote beta-End release induced by MSG may be involved in the mechanisms as well.
http://www.ncbi.nlm.nih.gov/m/pubmed/11938958/?i=2&from=/10374630/related
How can both of these things be true? Any ideas?