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How Psychedelic or Hallucinogenic Drugs Work

DisclaimerAll content on this website, including dictionary, thesaurus, literature, geography, and other reference data is for informational purposes only. This information should not be considered complete, up to date, and is not intended to be used in place of a visit, consultation, or advice of a legal, medical, or any other professional. Following the approval of a drug by the FDA, post marketing surveillance is conducted with the primary goal of monitoring long-term effects. Neuroplasticity is the brain’s ability to adapt, modify, and change structure through the growth and reorganization of neural networks in the organ. Psychedelics such as LSD, DMT, ketamine, and psilocybin have been found to promote neuroplasticity in animal brains (Ly et al., 2018), one of the reasons why they may provide a novel means of treating mood and anxiety disorders. Arthur Heffter first isolated and identified the compound in 1897, and it was first synthesized by Ernst Späth in 1918.

Of course, as reductionists, it is understood that the mystical experience must have neurochemical correlates. Even so, understanding what they are, how and why they occur, and how they lead to therapeutic improvement should shed light on the underlying deficits in brain function that lead to these disorders in the first place. Before-and-after brain imaging studies of patients with depression, anxiety, or addictive disorders will show how brain connectivity has changed as a result of psychedelic treatment. To understand these disorders at the present time with standard state-of-the-art approaches involves a sort of “fishing expedition,” searching for biomarkers that might be clues to the basis of the underlying disorder. Genome-wide association studies plow through many thousands or hundreds of thousands of genes, searching for candidates that might be the underlying causes of affective disorders. One generally cannot do prospective studies, to compare the brain function of the normal patient prior to the onset of his or her disease, and then examine it again after therapeutic improvement.

They demonstrated that DOI produced an anxiolytic effect only when microinjected into the hippocampus, but not into the amygdala or PAG. Indeed, when injected into the amygdala or PAG, DOI appeared to have an anxiogenic Psychedelic effect in the four-plates test, decreasing the number of punished crossings. In a subsequent study, Dave et al. examined the role of the hippocampus in 5HT2A receptor–mediated head bobs in the rabbit.

A later study of 5-HT2A receptor localization in the rat cortex by Miner et al. employed immunoperoxidase labeling to determine the localization of 5-HT2A receptors in the middle layers of the rat PFC. Using a polyclonal antibody, they found most 5-HT2A receptors to be expressed on postsynaptic structures, predominantly on proximal and distal dendritic shafts, apparently on both pyramidal and local circuit neurons. Most often, Miner et al. observed that 5-HT2A receptors were restricted to a particular area of the dendrite, usually extrasynaptic regions apposed to unlabeled dendrites. They reported that 73% of the immunopositive sites were postsynaptic, and 58% of those were on dendritic shafts, with 42% expressed in dendritic spines.

In a longitudinal study of 25,622 individuals with a history of substance involvement, Hendricks et al. found that use of psychedelics predicted a reduced likelihood of noncompliance with legal requirements that included alcohol and other drug use. The authors concluded that psychedelic use may promote alcohol and other drug abstinence as well as prosocial behavior in a population with high rates of recidivism. These investigators carried out an open-label proof-of-concept trial of psilocybin treatment in a sample of 10 volunteers with a DSM-IV diagnosis of alcohol dependence (Bogenschutz et al., 2014).