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Serotonergic psychedelic: Difference between revisions
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'''Serotonergic psychedelics''' (also known as '''serotonergic [[hallucinogen]]s''') are a class of [[hallucinogenic]] substances with a method of action strongly tied to modifying the normal [[neurotransmitter|neurotransmission]] of [[serotonin]] in the central nervous system (CNS). Serotonin, which is also referred to as '''5-HT''' (from its chemical name '''5'''-'''h'''ydroxy-'''t'''ryptamine) is a naturally-occurring [[monoamine neurotransmitter]] which is tied to developmental, cardiovascular, gastrointestinal, and endocrine function, sensory perception, behaviors such as aggression, appetite, sex, sleep, mood, cognition, and memory, many of which have yet to be fully understood.<ref>David E. Nichols and Charles D. Nichols, Serotonin Receptors. Chemical Reviews. 2008. 108 (5), 1614-1641. https://doi.org/10.1021/cr078224o</ref> | '''Serotonergic psychedelics''' (also known as '''serotonergic [[hallucinogen]]s''') are a class of [[hallucinogenic]] substances with a method of action strongly tied to modifying the normal [[neurotransmitter|neurotransmission]] of [[serotonin]] in the central nervous system (CNS). Serotonin, which is also referred to as '''5-HT''' (from its chemical name '''5'''-'''h'''ydroxy-'''t'''ryptamine) is a naturally-occurring [[monoamine neurotransmitter]] which is tied to developmental, cardiovascular, gastrointestinal, and endocrine function, sensory perception, behaviors such as aggression, appetite, sex, sleep, mood, cognition, and memory, many of which have yet to be fully understood.<ref>David E. Nichols and Charles D. Nichols, Serotonin Receptors. Chemical Reviews. 2008. 108 (5), 1614-1641. https://doi.org/10.1021/cr078224o</ref> | ||
== | ==Proposed method of action== | ||
[[File:Psilocybin neural connections.jpg|315px|thumbnail|right|The diagram above demonstrates the neural connections associated with sobriety in comparison to being under the influence of psilocybin as demonstrated through the use of MRI scans. The width of the links is proportional to their weight and the size of the nodes is proportional to their strength. Note that the proportion of heavy links between communities is much higher (and very different) in the psilocybin group, suggesting greater integration<ref>Petri, G., Expert, P., Turkheimer, F., Nutt, D., Hellyer, P. J., & Vaccarino, F. (2014). Homological scaffolds of brain functional networks, 14–18. https://doi.org/10.1038/nrn2618</ref>]] | [[File:Psilocybin neural connections.jpg|315px|thumbnail|right|The diagram above demonstrates the neural connections associated with sobriety in comparison to being under the influence of psilocybin as demonstrated through the use of MRI scans. The width of the links is proportional to their weight and the size of the nodes is proportional to their strength. Note that the proportion of heavy links between communities is much higher (and very different) in the psilocybin group, suggesting greater integration<ref>Petri, G., Expert, P., Turkheimer, F., Nutt, D., Hellyer, P. J., & Vaccarino, F. (2014). Homological scaffolds of brain functional networks, 14–18. https://doi.org/10.1038/nrn2618</ref>]] | ||
[[File:NeuroPsychDiagram.png|thumbnail|315px|right|Figure 1 - Activation of the prefrontal network and glutamate release by psychedelics. The figure shows a model in which hallucinogens, such as psilocin, lysergic acid diethylamide (LSD) and dimethyltryptamine (DMT), increase extracellular glutamate levels in the prefrontal cortex through stimulation of postsynaptic serotonin (5-hydroxytryptamine) 2A (5-HT 2A ) receptors that are located on large glutamatergic pyramidal cells in deep cortical layers (V and VI) projecting to layer V pyramidal neurons. This glutamate release leads to an activation of AMPA (α-amino-3-hydroxy-5-methyl-4- isoxazole propionic acid) and NMDA (N-methyl-d-aspartate) receptors on cortical pyramidal neurons. in addition, hallucinogens directly activate 5-HT2A receptors located on cortical pyramidal neurons. This activation is thought to ultimately lead to increased expression of brain-derived neurotrophic factor (BDNF).<ref>Vollenweider, F. X., & Kometer, M. (2010). The Neurobiology of Psychedelic Drugs: Implications for the Treatment of Mood Disorders. Nature Publishing Group, 11(9), 642–651. https://doi.org/10.1038/nrn2884</ref>]] | [[File:NeuroPsychDiagram.png|thumbnail|315px|right|Figure 1 - Activation of the prefrontal network and glutamate release by psychedelics. The figure shows a model in which hallucinogens, such as psilocin, lysergic acid diethylamide (LSD) and dimethyltryptamine (DMT), increase extracellular glutamate levels in the prefrontal cortex through stimulation of postsynaptic serotonin (5-hydroxytryptamine) 2A (5-HT 2A ) receptors that are located on large glutamatergic pyramidal cells in deep cortical layers (V and VI) projecting to layer V pyramidal neurons. This glutamate release leads to an activation of AMPA (α-amino-3-hydroxy-5-methyl-4- isoxazole propionic acid) and NMDA (N-methyl-d-aspartate) receptors on cortical pyramidal neurons. in addition, hallucinogens directly activate 5-HT2A receptors located on cortical pyramidal neurons. This activation is thought to ultimately lead to increased expression of brain-derived neurotrophic factor (BDNF).<ref>Vollenweider, F. X., & Kometer, M. (2010). The Neurobiology of Psychedelic Drugs: Implications for the Treatment of Mood Disorders. Nature Publishing Group, 11(9), 642–651. https://doi.org/10.1038/nrn2884</ref>]] | ||