Effects of LSD-25 on Relatives of Schizophrenic Patients

Anastasopoulos, George; Photiades, Harry

doi:10.1192/bjp.108.452.95

Cited by 33 publications

(8 citation statements)

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“…One of the most significant potential psychological side effects after the ingestion of psychedelic compounds in uncontrolled settings is the onset of a psychotic episode, which can last for several hours or days after the drug has worn off. The most vulnerable patients to the onset of long-lasting psychoses appear to be those who have previously received a diagnosis of SCZ, BD, or personality disorder or patients more inclined to mistrustfulness, fearfulness, and susceptibility on projection as defense (Anastasopoulos and Photiades, 1962;De Gregorio et al, 2016a. Other risk factors include mixing other psychoactive substances, such as cannabis.…”

Section: B Acute Side Effects Encountered In Uncontrolled Settingsmentioning

confidence: 99%

Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms

2020

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Mounting evidence suggests safety and efficacy of psychedelic compounds as potential novel therapeutics in psychiatry. Ketamine has been approved by the Food and Drug Administration in a new class of antidepressants, and 3,4-methylenedioxymethamphetamine (MDMA) is undergoing phase III clinical trials for post-traumatic stress disorder. Psilocybin and lysergic acid diethylamide (LSD) are being investigated in several phase II and phase I clinical trials. Hence, the concept of psychedelics as therapeutics may be incorporated into modern society. Here, we discuss the main known neurobiological therapeutic mechanisms of psychedelics, which are thought to be mediated by the effects of these compounds on the serotonergic (via 5-HT 2A and 5-HT 1A receptors) and glutamatergic [via N-methyl-D-aspartate (NMDA) and a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors] systems. We focus on 1) neuroplasticity mediated by the modulation of mammalian target of rapamycin-, brain-derived neurotrophic factor-, and early growth response-related pathways; 2) immunomodulation via effects on the hypothalamic-pituitaryadrenal axis, nuclear factor ĸB, and cytokines such as tumor necrosis factor-a and interleukin 1, 6, and 10 204 Inserra et al.

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Section: B Acute Side Effects Encountered In Uncontrolled Settingsmentioning

confidence: 99%

Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms

2020

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“…hallucinations and delusions) comparable to those seen in drug-naive first-episode schizophrenia patients (Geyer and Vollenweider, 2008; Gonzalez-Maeso and Sealfon, 2009b; Geyer et al, 2012) through a mechanism that involves activation of the 5-HT 2A receptor in cortical glutamatergic neurons (Beique et al, 2007; Gonzalez-Maeso et al, 2007; Celada et al, 2008). It has also been suggested that relatives of schizophrenic patients are more susceptible to the psychotic responses induced by LSD (Anastasopoulos and Photiades, 1962). Although LSD-like drugs as a model of psychosis have limitations (Hays and Tilley, 1973), these findings suggest that a better understanding of their molecular mechanism of action may provide additional insights into the brain processes underlying non-drug-induced psychoses.…”

Section: Pharmacological Models Of Psychosis and Antipsychotic Drug Amentioning

confidence: 99%

Preclinical models of antipsychotic drug action

Moreno

González-Maeso

2013

International Journal of Neuropsychopharmacology

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One of the main obstacles faced by translational neuroscience is the development of animal models of psychiatric disorders. Behavioural pharmacology studies indicate that psychedelic drugs, such as lysergic acid diethylamide (LSD) and dissociative drugs, such as phencyclidine (PCP), induce in healthy human volunteers psychotic and cognitive symptoms that resemble some of those observed in schizophrenia patients. Serotonin 5-HT2A and metabotropic glutamate 2 receptors have been involved in the mechanism of action of psychedelic and dissociative drugs. Here we review recent advances using LSD-like and PCP-like drugs in rodent models that implicate these receptors in the neurobiology of schizophrenia and its treatment.

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“…Hallucinogenic drugs aggravate psychosis in schizophrenia patients (Hoch et al, 1952). Of particular interest is also the finding of hallucinogenic (LSD)-induced psychotic symptoms in relatives of schizophrenic patients (Anastasopoulos and Photiades, 1962), suggesting that individuals with greater predisposition to schizophrenia are more susceptible to the psychotic responses that require activation of the 5-HT 2A R. In murine models, we and others have demonstrated that 5-HT 2A R-regulated pathways on cortical pyramidal neurons are necessary to mediate the signaling pattern and behavioral responses to hallucinogenic drugs (see [Gonzalez-Maeso and Sealfon, 2009] for review).…”

Section: Introductionmentioning

confidence: 99%

Dysregulated 5-HT2A receptor binding in postmortem frontal cortex of schizophrenic subjects

Muguruza

Moreno

Umali

et al. 2013

European Neuropsychopharmacology

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Previous postmortem and neuroimaging studies have repeatedly suggested alterations in serotonin 5-HT2A receptor (5-HT2AR) binding associated with the pathophysiology of schizophrenia. These studies were performed with ligands, such as ketanserin, altanserin and LSD, that may bind with high-affinity to different structural or functional conformations of the 5-HT2AR. Interpretation of results may also be confounded by chronic antipsychotic treatment and suicidal behavior in the schizophrenia group. We quantified 5-HT2AR density by radioligand binding assays in postmortem prefrontal cortex of antipsychotic-free (n=29) and antipsychotic-treated (n=16) schizophrenics, suicide victims with other psychiatric diagnoses (n=13), and individually matched controls. [3H]Ketanserin binding, and its displacement by altanserin or the LSD-like agonist DOI, was assayed. Results indicate that the number of [3H]ketanserin binding sites to the 5-HT2AR was increased in antipsychotic-free (128±11%), but not in antipsychotic-treated (92±12%), schizophrenic subjects. In suicide victims, [3H]ketanserin binding did not differ as compared to controls. Aging correlated negatively with [3H]ketanserin binding in schizophrenia, suicide victims and controls. The fraction of high-affinity sites of DOI displacing [3H]ketanserin binding to the 5-HT2AR was increased in antipsychotic-free schizophrenic subjects. Functional uncoupling of heterotrimeric G proteins led to increased fraction of high-affinity sites of altanserin displacing [3H]ketanserin binding to the 5-HT2AR in schizophrenic subjects, but not in controls. Together, these results suggest that the active conformation of the 5-HT2AR is up-regulated in prefrontal cortex of antipsychotic-free schizophrenic subjects, and may provide a pharmacological explanation for discordant findings previously obtained.

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Effects of LSD-25 on Relatives of Schizophrenic Patients

Cited by 33 publications

References 0 publications

Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms

Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms

Preclinical models of antipsychotic drug action

Dysregulated 5-HT2A receptor binding in postmortem frontal cortex of schizophrenic subjects

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