Neuroplasticity is the brain's ability to reorganize itself and adapt in response to changing environmental conditions or pathological stimuli. LSD is a potent psychedelic drug which has been able to rapidly stimulate neuroplasticity in animal studies. Various authors have speculated that changes in neuroplasticity may contribute to LSD's long-term effects, but there is still little direct evidence that LSD or other psychedelics enhance neuroplasticity in humans. The goal of this study is to investigate the effects of LSD on several measures of neuroplasticity in healthy human subjects.
Neuroplasticity is the brain's ability to reorganize itself and adapt in response to changing environmental conditions or pathological stimuli. Its dysregulation may play a role in the etiology of depression and anxiety disorders, and it is also essential for recovery from neural injury and stroke. LSD is a potent psychedelic drug and a member of the psychoplastogen family of small molecules, which are able to rapidly stimulate neuroplasticity in cortical neurons following a single dose. Previous research suggests that changes in neuroplasticity may contribute to LSD's long-term effects, which include increases in subjective well-being and life satisfaction, reduced anxiety, and increased openness to experience. Additionally, there is some evidence that LSD and other psychedelics could be viable clinical treatments for depression, anxiety, and addictive disorders, and that changes in neuroplasticity may underlie this clinical potential. However, there is still little direct evidence that LSD or other psychoplastogens enhance cortical plasticity in humans. The goal of this study is to investigate the effects of LSD on several measures of neuroplasticity in healthy human subjects, as well as other abilities and traits thought to be related to neuroplasticity. Determining whether LSD enhances cortical plasticity, how long this may last, where in the brain it occurs, and what it means for cognition and emotion is essential for understanding LSD's long-term effects, including but not limited to its clinical potential.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
100 micrograms LSD base
Low dose of LSD base
University of Fribourg
Fribourg, Canton of Fribourg, Switzerland
Change in motor evoked potential amplitude after paired associative stimulation (PAS)
Assessment of capacity for neuroplastic changes in the motor cortex
Time frame: Baseline, 8 hours post-treatment, 1 day post-treatment, 1 week post-treatment
Change in auditory event-related potential (ERP) amplitude after tetanic stimulation
Assessment of capacity for neuroplastic changes in the auditory cortex
Time frame: Baseline, 8 hours post-treatment, 1 day post-treatment, 1 week post-treatment
Plasma and serum levels of brain-derived neurotrophic factor (BDNF)
Marker of neuroplasticity
Time frame: Baseline, 8 hours post-treatment, 1 day post-treatment, 1 week post-treatment
Motor learning ability
Speed and accuracy on a motor learning task
Time frame: 1 day post-treatment
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QUADRUPLE
Enrollment
45