LSD via the 5-HT2A receptor (5-HT2AR), a subtype of serotonin receptor in the brain. LSD binds to this receptor and thereby causes specific changes in the regulation of certain proteins involved in cellular processes.
Proteostasis: The process by which cells correctly fold, maintain, and break down proteins. Impaired proteostasis can temporarily lead to increased cellular "plasticity," but prolonged disruption can be harmful.
Autophagy: The clearing of damaged cellular components. Downregulation of this can temporarily allow cell structures to persist that would normally be cleared — this may be related to neural restructuring.
mTOR signal path: Important for cell growth, synaptic plasticity, and memory formation.
DNA repair: Improved capacity to repair damaged DNA, which can have a neuroprotective effect.
Axon conduction: Supports the growth and reorientation of nerve endings — crucial for brain plasticity.
Synaptic vesicle fusion: Improves neurotransmission and communication between neurons.
Cellular energy metabolismEnsures sufficient energy during increased neural activity.
In short, LSD causes a brain state through activation of the 5-HT2A receptor in which synaptic plasticity, growth, and energy supply stimulated become, while clearing mechanisms are temporarily suppressed. This is likely one of the neurobiological foundations of the therapeutic effect of LSD within psychedelic therapy.