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Neurotrophic factors are molecules that enhance the growth and survival potential of neurons. They play important roles in both development, where they can act as guidance cues for developing neurons, and in the mature nervous system, where they are involved in neuronal survival, synaptic plasticity and the formation of long-lasting memories.
Moliner et al. show that psychedelics directly bind to the BDNF receptor TrkB with high affinity and promote BDNF-mediated plasticity and antidepressant-like effects, whereas their hallucinogenic-like effects are independent of TrkB binding.
The binding of psychedelics to the BDNF receptor TrkB boosts plasticity in cultured neurons and underlies the antidepressant-like effects of these compounds in mice.
Psychedelics induce fast and long-lasting antidepressant effects and neuronal plasticity, but their hallucinogenic effects limit their use. We show that, in mice, psychedelics bind directly to TrkB (the brain-derived neurotrophic factor (BDNF) receptor) with high affinity and promote BDNF-mediated plasticity and antidepressant-like effects, whereas their hallucinogenic-like effects are independent of TrkB binding.
This study suggests that brain-derived neurotrophic factor (BDNF) is released from dendritic spines in response to activity and acts in an autocrine manner to mediate structural plasticity of the spine from which it was released.
