SchizophreniaNeuroimaging & Brain Measures

Serotonin research: contributions to understanding psychoses

This review (2008) summarizes convergent evidence in support of the serotonergic model of psychedelics, schizophrenia, and psychosis, and concludes that the serotonergic system contributes to psychotic states only by interacting with other neurotransmitter systems in the brain.

Authors

  • Franz Vollenweider

Published

Trends in Pharmacological Sciences
meta Study

Abstract

The history of serotonin research is closely related to the study of hallucinogenic drugs that function as agonists at serotonin-2A receptors. The fundamental idea that psychotic states seen in psychiatric disorders such as schizophrenia might be attributable, in part, to abnormalities in serotonergic systems began with the almost simultaneous discovery of lysergic acid diethylamide (LSD), psilocybin and serotonin. Sixty years of study have confirmed early speculations regarding the important relationship between serotonin and both drug-induced and disorder-based psychotic states. Now, modern biochemical, pharmacological, behavioral, neuroimaging, genetic and molecular biological sciences are converging to understand how serotonergic systems interact with other monoaminergic and glutamatergic systems to modulate states of consciousness and contribute to psychotic disorders such as the group of schizophrenias. This review summarizes experimental assessments of the serotonergic hallucinogen model psychosis in relation to the serotonin hypothesis of schizophrenia.

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Research Summary of 'Serotonin research: contributions to understanding psychoses'

Introduction

Geyer and colleagues frame the historical link between serotonin (5-hydroxytryptamine, 5-HT) research and the study of psychoses through the discovery of both serotonin and serotonergic hallucinogens such as LSD and psilocybin. Early observations that these drugs produce psychosis-like subjective states led to the proposal that abnormalities in serotonergic systems could contribute to psychiatric disorders—particularly the schizophrenia spectrum—and that hallucinogens might serve as model psychoses. The introduction reviews phenomenological parallels between acute, drug-induced states and the early phases of schizophrenia, noting both similarities (changes in perception, thought, affect, and ego boundaries) and important differences (the lifelong course of schizophrenia versus rapid tolerance to hallucinogens; predominance of auditory hallucinations in schizophrenia versus visual phenomena with hallucinogens). The authors set out to summarise experimental assessments of the serotonergic hallucinogen model psychosis and to relate those findings to the serotonin hypothesis of schizophrenia. They indicate that modern methods from biochemistry, pharmacology, behavioural neuroscience, neuroimaging, genetics and molecular biology have converged to clarify how serotonergic systems interact with dopaminergic and glutamatergic neurotransmission to modulate consciousness and contribute to psychotic disorders. The review emphasises the relevance of these multi-level data to understanding early or acute psychotic states rather than the full chronic syndrome of schizophrenia.

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References (3)

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