Short answer: Emerging preclinical evidence suggests that some psychedelics, including LSD and psilocin, can interact with TrkB and enhance BDNF signaling, which is linked to plasticity-related cellular changes.
Most of this support comes from cell and animal studies. These data indicate that TrkB-mediated plasticity can be at least partly separable from classic 5-HT2A hallucinogenic signaling. However, mechanisms in humans are not yet confirmed, and results require independent replication and careful clinical translation.
For a concise overview of neuroplasticity in the context of psychedelics, see this article: neuroplasticity and psychedelics.
Hope this helps.