I'd imagine there wouldn't be any concern for SS as tianeptine doesn't increase the population of 5-ht in the synaptic clefts (according to this article*, tianeptine causes minimum if any alteration to the 5-ht neurotransmitter network. Doesn't increase firing rates of 5-ht neurons , didn't significantly decrease extracellular 5-ht levels [varies from area in brain i believe], or alter the the activity of 5-ht1a post-synaptic receptors. Essentially it doesn't fuck with the serotonergic system in a significant manner even with prolonged use as a therapeutic agent). Now I'd still be careful with say 2c-t-7 due to it's slight MAOi action, but I'm not sure if MAO's would oxidize tianeptine due to it's long amino-heptanoic chain as I'm not very knowledgeable on the metabolism of molecules via MAOi's. Taneptine also shows no affinity for any other known neurotransmitter receptors and does not inhibit the uptake noradrenaline in the central nervous system. Chronic tianeptine administration did not alter the concentration and affinity of α1A, α1B, α2A, α2B, α2C, β1, β2, 5-HT1, 5-HT2, 5-HT3, 5-HT4, 5-HT5A, 5-HT6, 5-HT7, NMDA, AMPA, kainate, benzodiazepine or GABA-B receptors, but increased the responsiveness of the α1-adrenergic system. Tianeptine does not inhibit MAOa and MAOb activity in the cortex, hippocampus, and hypothalamus. Systemic administration of tianeptine modestly enhanced the mesolimbic release of dopamine. The biological responses to tianeptine are presumably as a result of a cascade of effects, potentially/shown (certain functions) induced by the modulation of glutamate receptors (AMPA and NMDA). Glutamate has broad influence on other receptor systems, but it is thought that tianeptine's induced change in modulation of the glutamatergic system is a "normalization" of synaptic function. So, I couldn't really see it's modulation of glutamate receptors causing potential risks. Fuck, it really seems like it has a lot of potential behind it as very interesting molecule, even purely as a way to look farther into glutamatergic receptors influence on LTP, neurogensis, memory, stress, depression, etc.
So to sum this up, I don't think there would be any sort of interaction with psychedelics, but I'd avoid 2c-t-7 or other potential MAOi acting phenethylamines. I couldn't see it interacting with non-comp nmda antagonist, as it appears to be doing similar long term effects on the NMDAr system as say ketamine, through it's modulation of the receptor. I could even potentially see it being beneficial during a psychedelic experience as it has an inhibiting effect on the glutamate response of stress. Though, I'm just making a conjecture.
*
http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez
