Synthetic Psychedelic Phenethylamine Drugs After Microtubule Formation and Neurogenesis in Human Neural Progenitor Cells
Abstract
Understanding how psychedelic phenethylamines affect neural plasticity is essential in understanding effects associated with recreational drug use. Intracellular scaffolding proteins and downstream effectors, i.e., the microtubule cytoskeleton, have been proposed to modulate the effects of psychedelics. Microtubules are polymers of the protein tubulin that contribute to the cytoarchitecture, protein transport, and synaptic stability in cells. Our group has shown that psychedelic substituted phenethylamines interact with microtubules in a dose dependent manner to affect its ability to form. These interactions would prevent microtubule dependent protein transport within cells leading to altered cytoarchitecture of the cell and may be associated with adverse effects of psychedelic drugs. This study’s goal is to determine if the substituted phenethylamines 25B-NBF, 25C-NBF, and DMBMPP affect human neural progenitor cell (hNPC) proliferation, morphology, and survival. hNPCs were exposed to either 50 μM or 100 μM of each of the substituted phenethylamines or vehicle control for 24h. We hypothesize that substituted phenethylamine-induced altered microtubule formation leads to changes in hNPC proliferation, morphology, and survival. EdU cell proliferation assays and immunostaining were used to examine proliferation and cell cycle kinetics; TUNEL assays to examine programmed cell death; And, immunostaining to evaluate neurite formation and cellular morphology. Preliminary findings suggest hNPCs incubated with DMBMPP prevented neurite outgrowth, cell proliferation, and increased cell death. Identifying how substituted phenethylamine-induced changes in microtubule stability alter hNPCs may contribute to our understanding of how psychedelics produce different effects on behavior and identify therapeutic targets to treat their adverse effects.
Faculty Sponsors
Dr. James Munoz, Dr. Robert R. Smith, Dr. Travis J.A. Craddock
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-3-2024 12:30 PM
End Date
4-4-2024 1:30 PM
Synthetic Psychedelic Phenethylamine Drugs After Microtubule Formation and Neurogenesis in Human Neural Progenitor Cells
Alvin Sherman Library
Understanding how psychedelic phenethylamines affect neural plasticity is essential in understanding effects associated with recreational drug use. Intracellular scaffolding proteins and downstream effectors, i.e., the microtubule cytoskeleton, have been proposed to modulate the effects of psychedelics. Microtubules are polymers of the protein tubulin that contribute to the cytoarchitecture, protein transport, and synaptic stability in cells. Our group has shown that psychedelic substituted phenethylamines interact with microtubules in a dose dependent manner to affect its ability to form. These interactions would prevent microtubule dependent protein transport within cells leading to altered cytoarchitecture of the cell and may be associated with adverse effects of psychedelic drugs. This study’s goal is to determine if the substituted phenethylamines 25B-NBF, 25C-NBF, and DMBMPP affect human neural progenitor cell (hNPC) proliferation, morphology, and survival. hNPCs were exposed to either 50 μM or 100 μM of each of the substituted phenethylamines or vehicle control for 24h. We hypothesize that substituted phenethylamine-induced altered microtubule formation leads to changes in hNPC proliferation, morphology, and survival. EdU cell proliferation assays and immunostaining were used to examine proliferation and cell cycle kinetics; TUNEL assays to examine programmed cell death; And, immunostaining to evaluate neurite formation and cellular morphology. Preliminary findings suggest hNPCs incubated with DMBMPP prevented neurite outgrowth, cell proliferation, and increased cell death. Identifying how substituted phenethylamine-induced changes in microtubule stability alter hNPCs may contribute to our understanding of how psychedelics produce different effects on behavior and identify therapeutic targets to treat their adverse effects.
