Frontiers in Molecular Neuroscience
September 4, 2018
Rafael Vitor Lima Da Cruz, Thiago C. Moulin, Lyvia Lintzmaier Petiz et al.
86 citations
A single injection of the psychedelic compound 5-MeO-DMT into the brain's fluid-filled spaces increased the production of new neurons in the dentate gyrus of adult mice. Treated mice had more newborn granule cells, and these cells developed more complex branch-like structures. The new neurons also showed shorter afterhyperpolarization potentials and higher action potential thresholds, indicating altered electrical properties. These effects on neurogenesis may help explain the potential antidepressant actions of DMT-like compounds.
Frontiers in Molecular Neuroscience
September 11, 2015
Elena Enosyreva, Anita E Autry, Ege Ekavalali et al.
51 citations
Ketamine, an NMDA receptor antagonist, produces rapid antidepressant effects in adults with major depressive disorder by blocking NMDA receptors, which inhibits eukaryotic elongation factor 2 kinase, leading to increased protein synthesis and synaptic potentiation in the hippocampus. In juvenile animals, ketamine failed to produce an antidepressant response in the novelty suppressed feeding and forced swim tests and did not trigger synaptic potentiation in hippocampal slices, unlike in slices from older animals (6–9 weeks old). The NMDA receptor antagonist AP5 similarly triggered synaptic potentiation in mature hippocampus, indicating that global competitive blockade of NMDA receptors is sufficient for this effect. These findings suggest that global NMDA receptor blockade in developmentally mature hippocampal synapses is necessary for ketamine's antidepressant efficacy.
Frontiers in Molecular Neuroscience
December 24, 2021
Lynette A. Desouza, Madhurima Benekareddy, Sashaina E. Fanibunda et al.
46 citations
The hallucinogenic compound DOI, which activates the 5-HT2A receptor, rapidly increases the expression of several genes linked to neuronal plasticity in rat cortical neurons and neocortex. This upregulation involves the transcription factor CREB, which becomes phosphorylated through MAP kinase and CaMKII signaling pathways. DOI enhanced CREB binding to specific gene promoters (Arc, Bdnf1, Cebpb, cFos) but not others (Egr1, Egr2). In mice lacking CREB, DOI-induced expression of Arc, cFos, and Cebpb was significantly reduced. The findings suggest that serotonergic psychedelics may recruit CREB to drive rapid psychoplastogenic effects, similar to slower-acting antidepressants.
Frontiers in Molecular Neuroscience
October 12, 2021
Kacper Łukasiewicz, Jacob J. Baker, Yi Zuo et al.
32 citations
Psychedelics, which have been used for centuries, can dramatically alter conscious experience. Recent research indicates that certain psychedelics promote neural plasticity by stimulating neurite growth and synapse formation. This review concentrates on classical serotonergic psychedelics and their role in neural plasticity, discussing how this mechanism may underlie their therapeutic potential.
Frontiers in Molecular Neuroscience
April 4, 2019
Rafael Vitor Lima Da Cruz, Thiago C. Moulin, Lyvia Lintzmaier Petiz et al.
4 citations
correction
This is a correction notice for a previously published article. It does not present new findings or arguments. The notice corrects errors in the original paper, specifically in the Materials and Methods section regarding the number of animals used per group and in the Results section regarding the number of animals per group for behavioral tests.