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Keer He

Department of Chemistry, Columbia University, New York, New York 10027, United States.

3 papers in the library · 24 citations · publishing 2024-2025

Papers

Molecular Design of SERTlight: A Fluorescent Serotonin Probe for Neuronal Labeling in the Brain.

Journal of the American Chemical Society April 10, 2024 Wei-Li Lee, Xavier Westergaard, Christopher Hwu et al. 18 citations

A novel small molecule fluorescent agent called SERTlight specifically labels serotonin neurons in the mammalian brain. SERTlight is a substrate for the serotonin transporter (SERT) and accumulates inside serotonin neurons, producing a bright and selective optical signal. Unlike many other agents, SERTlight does not activate serotonin receptors or other common targets and is not released by neuronal activity or drugs like MDMA. It is compatible with other imaging tools and can label distant axonal projections while allowing simultaneous measurement of serotonin release. This new tool enables detailed study of the serotonin system in health and disease.

Robust Methods For Quantifying Neuronal Morphology And Molecular Signaling Reveal That Psychedelics Do Not Induce Neuroplasticity

bioRxiv Preprint Server March 4, 2024 Umed Boltaev, Hyun W. Park, Keaon R. Brown et al. 4 citations preprint

Classic psychedelics are thought to work by inducing neuroplasticity, often measured as dendritic arbor growth. This study tested whether psychedelics directly activate the TrkB receptor or BDNF/TrkB signaling, and whether they cause morphological growth in primary cortical neurons. Using a multimodal screening platform, the authors found that psychedelics do not directly modulate TrkB or BDNF-TrkB signaling, and that 5-HT2A receptor expression and functional levels are low. Psychedelics did not induce dendritogenesis, unlike BDNF which did. These results challenge previous findings and highlight the need for rigorous methods in studying neuroplasticity.

Deciphering Ibogaine’s Matrix Pharmacology: Multiple Transporter Modulation at Serotonin Synapses

Journal of the American Chemical Society December 26, 2025 Christopher Hwu, Václav Havel, Xavier Westergaard et al. 2 citations

Ibogaine and its main metabolite noribogaine inhibit the vesicular monoamine transporter 2 (VMAT2) with submicromolar potency, as shown in cell-based assays and two-photon microscopy of mouse brain synaptic vesicle clusters. Noribogaine also induces partial serotonin release from synaptic vesicles and binds VMAT2 at a distinct site from the established inhibitor dihydrotetrabenazine. These compounds additionally inhibit plasma membrane monoamine transporters, prominently the serotonin transporter (SERT), and a novel target, organic cation transporter 2 (OCT2). Several iboga analogs display dual inhibition of VMAT2 and SERT with comparable potencies, termed "Synaptic Reuptake Inhibitors" (SynRIs). This profile explains why ibogaine and noribogaine do not induce catalepsy, unlike other VMAT2 inhibitors, and illustrates the complex "matrix pharmacology" of iboga compounds.