This early (1997) study looked at the effects of psylocybin/psilocin in the brain through a PET scan and found increases in metabolis (CMRglu) that correlated with the experienced ‘psychotic’ (psychedelic) effects.
Abstract of Positron emission tomography and fluorodeoxyglucose studies of metabolic hyperfrontality and psychopathology in the psilocybin model of psychosis
“The effects of the indolehallucinogen psilocybin, a mixed 5-HT2 and 5-HT1 agonist, on regional cerebral glucose metabolism were investigated in 10 healthy volunteers with PET and [F-18]-fluorodeoxyglucose (FDG) prior to and following a 15-or 20-mg dose of psilocybin. Psychotomimetic doses of psilocybin were found to produce a global increase in cerebral metabolic rate of glucose (CMRglu) with significant and most marked increases in the frontomedial and frontolateral cortex (24.3%), anterior ungulate (24.9%), and temporomedial cortex (25.3%). Somewhat smaller increases of CMRglu were found in the basal ganglia (18.5%), and the smallest increases were found in the sensorimotor (14.7%) and occipital cortex (14.4%). The increases of CMRglu in the prefrontal cortex anterior cingulate, temporomedial cortex, and putamen correlated positively with psychotic symptom formation, in particular with hallucinatory ego disintegration. The present data suggest that excessive 5-HT2 receptor activation results in a hyperfrontal metabolic pattern that parallels comparable metabolic findings associated with acute psychotic episodes in schizophrenics and contrasts with the hypofrontality in chronic schizophrenic patients.”
Authors: Franz X. Vollenweider, Klaus L. Leenders, Christian Scharfetter, Philip Maguire, Otto Stadelmann, Jules Angst
Summary of Positron emission tomography and fluorodeoxyglucose studies of metabolic hyperfrontality and psychopathology in the psilocybin model of psychosis
Psilocybin, a mixed S-HT, and 5-HT, agonist, increased cerebral metabolic rate of glucose in 10 healthy volunteers, with the greatest increases found in the prefrontal cortex, anterior cingulate, temporomedial cortex, and putamen. This increase correlated positively with psychotic symptom formation.
Psilocybin and LSD are potent indolehallucinogens that can induce a psychosis-like syndrome in humans that resembles in various aspects the first manifestation of schizophrenia. The serotonergic system may play a critical role in the pathophysiology of schizophrenia.
In the present PET and FDG study, we take advantage of the psilocybin model of psychosis to examine the associations between serotonin receptor activation, acute psychotic symptom formation, and metabolic alterations in the living human brain. Several PET studies have found metabolic hypofrontality in chronic schizophrenic patients, but some studies could not confirm this finding. These studies investigated mainly subacute schizophrenics, and some studies demonstrated hypertemporality, a left-right asymmetry of metabolism, and increased or reduced metabolism in the basal ganglia.
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https://doi.org/10.1016/S0893-133X(96)00246-1
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Cite this paper (APA)
Vollenweider, F. X., Leenders, K. L., Scharfetter, C., Maguire, P., Stadelmann, O., & Angst, J. (1997). Positron emission tomography and fluorodeoxyglucose studies of metabolic hyperfrontality and psychopathology in the psilocybin model of psychosis. Neuropsychopharmacology, 16(5), 357-372.
Study details
Compounds studied
Psilocybin
Topics studied
Schizophrenia
Study characteristics
Open-Label
Bio/Neuro
Participants
15
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