oh it's certainly a neurotransmitter, binding metabotropic (G-coupled) receptors, whether endogenous or exogenous; this isn't really disputable. it's a competitive ligand at active binding sites, and thus initiates signal transduction as such.

DMTs function is to show you the other side rather then this side.

But this isn't the definition of neurotransmiter, no?

A "neurotransmitter" has to be released from presynaptic neuron with an aim to bind to an try to depolarise the post-synaptic one. Neurotransmiters are by definition released in the synapses. Norepinephrine is a neurotransmiter but epinephrine is not; epinephrine is an endocrine hormone and not neurotransmitter since it is not released in the synapsis.

Is there a publication that shows dmt to be released in the synapsis?

not that i'm aware of; hmm...so what is it, a pseudo-neurotransmitter? it would still be
a secondary messenger
yea, i forgot that neurotransmitters are packed into vesicles, which fuse with the presynaptic-membrane following Ca2+ influx.

if epinephrine is a hormone, that would make it a primary messenger (neurotransmitters are secondary messengers).

From an adaptation standpoint, and Shulgin has also mentioned this in Dirty Pictures, it may just be that over the course of human evolution, the human brain developed metabolic pathways to supress endogenous psychedelic ligands...a sort of filter mechanism...for self preservation, survival as a species.

The plant hallucinogen N,N-dimethyltryptamine (DMT) has been used for religious and other purposes for many centuries. The psychological effects of ingested DMT are characterized as an intense dream-like state with fantastic visual imagery, altered time and space perceptions, changes in body image and sensations, and feelings ranging from euphoria to sadness to amazement. Over the past several decades, scientists have linked the psychoactive effects of DMT to various neurochemical processes including action at serotonin receptors and transporters and monoamine oxidase enzymes.
We recently identified the sigma-1 receptor as the latest molecular target for DMT. We reported that DMT binds to sigma-1 receptors at low micromolar concentrations, inhibits sigma-1 receptor-regulated sodium ion channels at higher concentrations, and induces a hypermobility response in wild-type mice that is abolished in sigma-1 receptor knockout mice (Fontanilla 2009). In a later study, we reported that DMT and other psychedelic tryptamines exhibit substrate behavior at plasma membrane and synaptic vesicle uptake transporters (Cozzi 2009). We hypothesize that these uptake processes may allow the accumulation of DMT within neurons to reach relatively high levels and, when stored in synaptic vesicles, to function as a releasable transmitter. We have now obtained direct experimental evidence in support of this hypothesis by observing that DMT can be taken up by model neuronal cells (PC12 cells) and subsequently released by these cells under conditions of controlled depolarization. The psychedelic effects of DMT and related compounds likely arise from a complex interplay among all of these enzyme, receptor, and transporter mechanisms.

While that could be true, consider the forward-looking, flip side of that statement: an opportunity in our future evolution - possibly a necessity if we're not going to blow ourselves to smithereens - is to develop the metabolic pathways to encourage endogenous psychedelic ligands.

A number of Buddhist practitioners I know believe, for example, that the "relics" known as sarira or ringsel, found in the cremated remains of teachers they consider "spiritually advanced", are connected to the change in the amino acids in their bodies that arise from many years of meditation and spiritual practices

I could imagine that in a sense we're always under the influence of endogenous tryptamine psychedelic's, but just to such a limited degree that we normally don't notice it.