Increased activation of indirect semantic associations under psilocybin

Spitzer, Manfred; Thimm, Markus; Hermle, Leo; Holzmann, Petra; Kovar, Karl‐Artur; Heimann, H; Gouzoulis-Mayfrank, Euphrosyne; Kischka, Udo; Schneider, Frank

doi:10.1016/0006-3223(95)00418-1

Cited by 86 publications

(84 citation statements)

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“…As previously reported, psilocybin given to healthy volunteers produced changes in mood, disturbances in thinking, illusions, elementary and complex visual hallucinations, as well as impairment of ego-functioning (Heimann 1986;Spitzer et al 1996;Vollenweider et al 1997). Most prominent among these symptoms were derealisation and depersonalisation associated with heightened mood or euphoria (OSE).…”

Section: Discussionmentioning

confidence: 65%

“…Particularly, ego-disorders (Rüm-mele and Gnirss 1961;Vollenweider et al 1997), affective changes (Rümmele and Gnirss 1961), loosened associations (Spitzer et al 1996) and perceptual alterations commonly seen in psilocybin-induced psychosis are also observed in incipient acute schizophrenic stages (Bowers and Freedman 1966;Heimann, 1986;Gouzoulis et al 1994). In support of these suggested clinical similarities, we recently found that psilocybin produced a marked prefrontal and anterior cingulate activation in normal subjects comparable to the hyperfrontal pattern observed in some (Cleghorn et al 1989;Ebmeier et al 1993Ebmeier et al , 1995Catafau et al 1994;Parellada et al 1994;Ebmeier et al 1995;Sabri et al 1997) but not all (Andreasen et al 1992;Buchsbaum et al 1992;Liddle et al 1992;Siegel et al 1993) acute schizophrenic patients.…”

Section: The Modulating Effects Of Serotonin On Dopamine Neurotransmimentioning

confidence: 99%

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5-HT Modulation of Dopamine Release in Basal Ganglia in Psilocybin-Induced Psychosis in Man—A PET Study with [11C]raclopride

Vollenweider

1999

Neuropsychopharmacology

253

138

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The modulating effects of serotonin on dopamine neurotransmission are not well understood, particularly in acute psychotic states. Positron emission tomography was used to examine the effect of psilocybin on the in vivo binding of [ 11 C]raclopride to D 2 -dopamine receptors in the striatum in healthy volunteers after placebo and a psychotomimetic dose of psilocybin (n ϭ 7). Psilocybin is a potent indoleamine hallucinogen and a mixed 5-HTPsilocybin, a potent indoleamine hallucinogen and 5-HT receptor stimulating agent, has been reported to produce a psychosis-like syndrome in man resembling the first manifestation of schizophrenia in certain respects [for review see (Fischman 1983;Gouzoulis-Mayfrank et al. 1998)]. Particularly, ego-disorders (Rüm-mele and Gnirss 1961;Vollenweider et al. 1997), affective changes (Rümmele and Gnirss 1961), loosened associations (Spitzer et al. 1996) and perceptual alterations commonly seen in psilocybin-induced psychosis are also observed in incipient acute schizophrenic stages (Bowers and Freedman 1966;Heimann, 1986;Gouzoulis et al. 1994). In support of these suggested clinical similarities, we recently found that psilocybin produced a marked prefrontal and anterior cingulate activation in normal subjects comparable to the hyperfrontal pattern observed in some (Cleghorn et al. 1989;Ebmeier et al. 1993Ebmeier et al. , 1995Catafau et al. 1994 1994;Ebmeier et al. 1995;Sabri et al. 1997) but not all (Andreasen et al. 1992;Buchsbaum et al. 1992;Liddle et al. 1992;Siegel et al. 1993) acute schizophrenic patients. A number of functional animal studies have suggested that indoleamine (psilocybin, LSD) and phenylethylamine (DOI, mescaline) hallucinogens produce their psychotomimetic effects primarily through excessive stimulation of 5-HT, and 5-HT 2A receptors in particular (McKenna et al. 1989;Pierce and Peroutka 1989;Aghajanian 1994;Sipes and Geyer 1994;Padich et al. 1996). This assumption was corroborated in a recent human study demonstrating that the psychotomimetic effects of psilocybin can be blocked dose-dependently by pretreatment with the preferential 5-HT 2A receptor antagonist ketanserin (Vollenweider et al. 1998). However, pretreatment with the D 2 -antagonist haloperidol also reduces some of the positive symptoms of psilocybin psychosis. This raises the possibility that symptoms of psilocybin are secondary responses to increased dopaminergic transmission (Vollenweider et al. 1998).Hence, a contribution of the dopamine systems to the effects of psilocybin, presumably through a serotonindopamine interaction, cannot be ruled out. Functional interactions between central serotonin (5-HT) and dopamine (DA) systems have been well documented. Electrophysiological, biochemical, and behavioral evidence suggests that the ascending serotonergic pathways from the medial and dorsal raphe modulate or control the function of the mesolimbic and mesostriatal dopamine systems (Joyce 1993;Zazpe et al. 1994;Kapur and Remington 1996). The modulating effect of serotonin on striatal dopamine release...

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Section: Discussionmentioning

confidence: 65%

Section: The Modulating Effects Of Serotonin On Dopamine Neurotransmimentioning

confidence: 99%

5-HT Modulation of Dopamine Release in Basal Ganglia in Psilocybin-Induced Psychosis in Man—A PET Study with [11C]raclopride

Vollenweider

1999

Neuropsychopharmacology

253

138

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“…Hallucinogens induce formal thought disturbances with loosening of associations. Indirect semantic priming, an index of spreading activation in semantic networks, was reported to be increased in healthy volunteers after ingestion of psilocybin (Spitzer et al 1996). 3.…”

Section: The Neurometabolic Effects Of the Hallucinogen Psilocybin (Pmentioning

confidence: 98%

Neurometabolic Effects of Psilocybin, 3,4-Methylenedioxyethylamphetamine (MDE) and d-Methamphetamine in Healthy Volunteers A Double-Blind, Placebo-Controlled PET Study with [18F]FDG

Gouzoulis-Mayfrank

1999

Neuropsychopharmacology

178

100

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The neurometabolic effects of the hallucinogen psilocybin (PSI; 0.2 mg/kg), the entactogen 3,4-methylenedioxyethylamphetamine (MDE; 2 mg/kg) and the stimulant d-methamphetamine (METH; 0.2-0.4 mg/kg) and the drugs' interactions with a prefrontal activation taskwere investigated in a double-blind, placebo-controlled human [F-18]fluorodeoxyglucoseFDG-positron emission tomographicPET study (each group: n ϭ 8 Experimental studies of cerebral blood flow and metabolism with psychoactive drugs in humans aim to explore the interaction of these drugs with human brain function. Recent studies with hallucinogenic, "mind-expanding" drugs in healthy subjects provided evidence in favor of an altered functional interhemispheric balance From the Department of Psychiatry and Psychotherapy (EG-M, BT, HS), University of Technology (RWTH), Aachen, Germany; Department of Nuclear Medicine (MS, OS, CA, UB), University of Technology (RWTH), Aachen, Germany; Department of Psychiatry (MS), University of Ulm, Ulm, Germany; Pharmaceutical Institute (K-AK), University of Tübingen, Tübingen, Germany; Psychiatric and Neurological Hospital Christophsbad (LH), Göppingen, Germany.Address correspondence to: E. Gouzoulis-Mayfrank, M.D., Department of Psychiatry and Psychotherapy, University of Technology (RWTH), Pauwelsstrasse 30, D-52074 Aachen, Germany.Received March 14, 1998, accepted July 20, 1998 566 E. Gouzoulis-Mayfrank et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 6 with right hemispheric dominance and an increased activity in frontocortical regions after acute administration of mescaline, psilocybin, or ketamine (Hermle et al. 1992; Vollenweider et al. 1997a, b). The most profound increase in metabolism was found in the anterior cingulate (Vollenweider et al. 1997a(Vollenweider et al. , 1997b, which is linked to both emotional and attentional functions (Vogt et al. 1992;Devinsky et al. 1995;Murtha et al. 1996). These functions are, in turn, tightly connected to both the effects of hallucinogens and the symptoms of schizophrenic and schizophrenia-spectrum psychoses.Hallucinogenic drug-induced states can be used as models for acute endogenous psychotic states in psychiatric research (Hermle et al. 1992; Vollenweider et al. 1997a, b;Gouzoulis-Mayfrank et al. 1998). Within the framework of this model psychosis paradigm neurometabolic data from the above-mentioned studies can be interpreted in the sense that acute psychotic states with prominent positive symptoms are linked to increased activity in frontal neocortical, and limbic areas. This is in contrast to the majority of functional neuroimaging studies with schizophrenic patients, which demostrate hypofrontality both in resting states (Buchsbaum et al. 1982;Farkas et al. 1984;Wolkin et al. 1988;Siegel et al. 1993) and under cognitive tasks believed to employ frontal brain areas (Cohen et al. 1987;Weinberger et al. 1988;Buchsbaum et al. 1990;Andreasen et al. 1992). However, most of these studies were performed with chronically ill patients on various neuroleptic medications, a...

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“…Spitzer et al (1996) demonstrated indirect semantic priming effects which appeared to parallel plasma levels of an active metabolite after administration of psilocybin (an indolealkylamine hallucinogen with multiple monoaminergic effects) to eight normal participants. Kischka et al (1996) found exogenous l-DOPA to decrease the indirect semantic priming effect observed relative to placebo-administered control semantic priming effects, in 31 normal participants performing an LDT with either an SOA of 200 or 700 ms.…”

Section: The Role Of Monoamines In Semantic Priming Effectsmentioning

confidence: 99%

Semantic priming in schizophrenia: A review and synthesis

Minzenberg

Ober

Vinogradov

2002

J Int Neuropsychol Soc

132

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In this paper, we present a review of semantic priming experiments in schizophrenia. Semantic priming paradigms show utility in assessing the role of deficits in semantic memory network access in the pathology of schizophrenia. The studies are placed in the context of current models of information processing. In this review we include all English-language reports (from peer-reviewed journals) of single-word semantic priming studies involving participants with schizophrenia. The studies to date show schizophrenic patients to exhibit variable semantic priming effects under automatic processing conditions, and consistent impairments under controlled0attentional conditions. We also describe associations with other neurocognitive dysfunction, neurochemical and electrophysiological disturbances, and clinical manifestations (such as thought disorder).

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Increased activation of indirect semantic associations under psilocybin

Cited by 86 publications

References 7 publications

5-HT Modulation of Dopamine Release in Basal Ganglia in Psilocybin-Induced Psychosis in Man—A PET Study with [11C]raclopride

5-HT Modulation of Dopamine Release in Basal Ganglia in Psilocybin-Induced Psychosis in Man—A PET Study with [11C]raclopride

Neurometabolic Effects of Psilocybin, 3,4-Methylenedioxyethylamphetamine (MDE) and d-Methamphetamine in Healthy Volunteers A Double-Blind, Placebo-Controlled PET Study with [18F]FDG

Semantic priming in schizophrenia: A review and synthesis

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