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March 2024
ROBUST METHODS FOR QUANTIFYING NEURONAL
MORPHOLOGY AND MOLECULAR SIGNALING REVEAL THAT
PSYCHEDELICS DO NOT INDUCE NEUROPLASTICITY
Umed Boltaev1, Hyun W. Park1, Keaon R. Brown1, Maya Delgado1, Jorryn Wu1,
Brianna N. Diaz-Pacheco1, Maria Botero Pinzon1, Keer He1, Erin Ahern1, Nina Goldshmid1,
Eleanor H. Simpson2,3, and Dalibor Sames1,4
1. Department of Chemistry, Columbia University, New York, NY, USA.
2. New York State Psychiatric Institute, New York, NY, USA
3. Department of Psychiatry, Columbia University, New York, NY, USA
4. Zuckerman Mind Brain Behavior Institute, Center at Columbia University, New York, NY,
USA
Corresponding authors:
Umed Boltaev: umed.boltaev@columbia.edu
Dalibor Sames: ds584@columbia.edu
.CC-BY-NC-ND 4.0 International licenseavailable under a
(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made
The copyright holder for this preprintthis version posted March 8, 2024.;https://doi.org/10.1101/2024.03.04.583022doi:bioRxiv preprint
and sustained therapeutic effects of classic psychedelics. Within this broad concept,
examination of morphological neuronal plasticity, such as dendritic arbor growth, is widely used
to assess the neuroplasticity effects of classic and novel psychedelics. At the molecular level, it
has been reported that serotonergic psychedelic compounds mediate dendritogenesis via the
master molecular regulator of plasticity, TrkB, either directly via BDNF/TrkB signaling
potentiation or indirectly through 5-HT2A receptor. To examine these hypotheses in detail, we
developed a robust multimodal screening platform for unbiased, semi-automated quantification
of cellular morphology and multiplex molecular signaling in the same cortical neurons. We found
that in widely used primary neuronal cultures psychedelics do not directly modulate TrkB
receptor or BDNF-TrkB signaling. We also found 5HT2a receptor gene expression and
functional receptor levels are low, and psychedelics do not induce morphological growth, in
contrast to significant dendritogenesis elicited by BDNF. Our results challenge recently
published results in the field and indicate a need for rigorous experimental methods to study
morphological manifestations of neuroplasticity effects induced by clinically used and
experimental therapeutics.
Brianna N. Diaz-Pacheco1, Maria Botero Pinzon1, Keer He1, Erin Ahern1, Nina Goldshmid1,
Eleanor H. Simpson2,3, and Dalibor Sames1,4
1. Department of Chemistry, Columbia University, New York, NY, USA.
2. New York State Psychiatric Institute, New York, NY, USA
3. Department of Psychiatry, Columbia University, New York, NY, USA
4. Zuckerman Mind Brain Behavior Institute, Center at Columbia University, New York, NY,
USA
Corresponding authors:
Umed Boltaev: umed.boltaev@columbia.edu
Dalibor Sames: ds584@columbia.edu
.CC-BY-NC-ND 4.0 International licenseavailable under a
(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made
The copyright holder for this preprintthis version posted March 8, 2024.;https://doi.org/10.1101/2024.03.04.583022doi:bioRxiv preprint
Abstract
Induction of neuroplasticity has become the dominant explanatory framework for the rapidand sustained therapeutic effects of classic psychedelics. Within this broad concept,
examination of morphological neuronal plasticity, such as dendritic arbor growth, is widely used
to assess the neuroplasticity effects of classic and novel psychedelics. At the molecular level, it
has been reported that serotonergic psychedelic compounds mediate dendritogenesis via the
master molecular regulator of plasticity, TrkB, either directly via BDNF/TrkB signaling
potentiation or indirectly through 5-HT2A receptor. To examine these hypotheses in detail, we
developed a robust multimodal screening platform for unbiased, semi-automated quantification
of cellular morphology and multiplex molecular signaling in the same cortical neurons. We found
that in widely used primary neuronal cultures psychedelics do not directly modulate TrkB
receptor or BDNF-TrkB signaling. We also found 5HT2a receptor gene expression and
functional receptor levels are low, and psychedelics do not induce morphological growth, in
contrast to significant dendritogenesis elicited by BDNF. Our results challenge recently
published results in the field and indicate a need for rigorous experimental methods to study
morphological manifestations of neuroplasticity effects induced by clinically used and
experimental therapeutics.
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