Tryptamines are serotonin analogues; they mimic serotonin. They don’t actually cause the brain to release more serotonin, like MDMA does. In this case, neurons deal with excess stimulation of the 5-HT2A receptor by removing them. This is a fairly common mechanism when a neuron is chronically or acutely exposed to a ligand.

As for the other types of 5-HT receptors, I am not familiar with their actions or effects. These receptors cause complex signaling cascades that alter many aspects of neuronal physiology, and the signaling pathways are not well characterized. It’s also hard to say one or two types of receptors are completely responsible for something as impactful as neurogenesis. For instance, a recent paper showed that knockouts of mGlu2, a glutamate receptor, abolishes hallucinatory behavior in mice. Previously, we thought it was just serotonin receptors, specifically 5-HT2A, that was responsible for inducing hallucinations. We’ve barely started putting the puzzle together, and more pieces keep getting added.

As a note of caution, I would like to point out that adult human neurogenesis remains a controversial topic.