Serotonergic hallucinogens as translational models relevant to schizophrenia
The International Journal of Neuropsychopharmacology – August 13, 2013
Source: OpenAlex
Summary
Compelling evidence links serotonergic hallucinogens like psilocybin, mescaline, and lysergic acid diethylamide to temporary psychosis, mimicking schizophrenia symptoms. These psychedelics influence behavior by targeting the serotonin 5-HT2A neurotransmitter receptor. This neurochemical interaction provides crucial insights for Psychology and Neuroscience, particularly within Drug Studies. Understanding how these substances induce a 'model psychosis' through specific receptor influence, revealed by biochemical analysis, helps unravel schizophrenia's pathogenesis. This knowledge is vital for developing novel therapeutic approaches.
Abstract
Abstract One of the oldest models of schizophrenia is based on the effects of serotonergic hallucinogens such as mescaline, psilocybin, and (+)-lysergic acid diethylamide (LSD), which act through the serotonin 5-HT2A receptor. These compounds produce a ‘model psychosis’ in normal individuals that resembles at least some of the positive symptoms of schizophrenia. Based on these similarities, and because evidence has emerged that the serotonergic system plays a role in the pathogenesis of schizophrenia in some patients, animal models relevant to schizophrenia have been developed based on hallucinogen effects. Here we review the behavioural effects of hallucinogens in four of those models, the receptor and neurochemical mechanisms for the effects and their translational relevance. Despite the difficulty of modelling hallucinogen effects in nonverbal species, animal models of schizophrenia based on hallucinogens have yielded important insights into the linkage between 5-HT and schizophrenia and have helped to identify receptor targets and interactions that could be exploited in the development of new therapeutic agents.