Posted 23 June 2015 - 12:14 AM
Are the cortisol-lowering effects from phosphatidylserine due to its eventual breakdown into D-serine from L-serine or is the phosphatidylserine molecule responsible on its own? I can't seem to find info on this. Or another way to put this question is, would agonizing the NMDA receptor at the glycine site lower cortisol? Any help is appreciated.
Posted 23 June 2015 - 02:56 AM
I did find this:
http://www.ncbi.nlm....pubmed/11282259
"As prolactin and cortisol liberation is in part influenced through NMDA-receptors we investigated whether the elevation of prolactin or cortisol plasma levels is a class effect of NMDA-antagonists and might be an appropriate marker for studying NMDA-antagonistic potency."
"Ketamine increased serum prolactin and cortisol levels (p < 0.001), whereas memantine and placebo did not affect hormone levels."
If Ketamine, an NMDA antagonist can increase cortisol, then D-serine, an agonist of NMDA, should decrease it? Tell me if my thoughts on this are wrong.
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