Psychedelics have sparked widespread interest in their potential therapeutic benefits, particularly in the treatment of anxiety and mood disorders. According to research, these compounds may boost neuroplasticity and encourage the formation of new synaptic connections, particularly in the hippocampus, a brain region responsible for memory and emotion regulation.
A traditional psychedelic, such as LSD, psilocybin, and mescalin, was shown to activate a cell type in the brain that silences other surrounding neurons, providing insight into how such drugs relieve anxiety, according to a recent study.
The findings show the psychedelic DOI (2,5-dimethoxy-4-iodoamphetamine) lessened anxiety in mice and rats while activating the ventral hippocampus and so-called fast-spiking interneurons there.
It hasn’t been known what brain areas and cell types are involved when psychedelics suppress anxiety. The idea is that if we know the neurobiology involved, we can design some better drug that would target these pathways.
Alex Kwan
“It hasn’t been known what brain areas and cell types are involved when psychedelics suppress anxiety,” said Alex Kwan, associate professor of biomedical engineering at Cornell University and senior author of the study, which published in the journal Neuron. “The idea is that if we know the neurobiology involved, we can design some better drug that would target these pathways.”
“The work provides an understanding of the cellular trigger for the psychedelic-induced relief of anxiety,” said Vidita Vaidya, senior professor of biological sciences at the Tata Institute of Fundamental Research in Mumbai, and the paper’s corresponding author.
The pathway in the ventral hippocampus – a brain structure involved in social memory, emotion, and affect – does not appear to cause the hallucinations associated with DOI, implying that some of the therapeutic effects of psychedelics, such as reducing PTSD, depression, and anxiety, may be isolated within discrete brain circuits, according to Vaidya.
“That opens up the possibility to design psychedelic inspired drugs that target anxiety without evoking potent hallucinations,” according to her.
The study builds on earlier research that identified abnormal hyperactivity in the ventral hippocampus when an animal is anxious, particularly neurons that communicate with the amygdala, the major processing center for emotions.
“There’s a hint that in the anxiety state, these cells are active, and maybe the drug works by then silencing some of these,” Kwan said.
