Model psychosis

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The term model psychosis (synonym: experimental psychosis ) describes psychosis-like experiences that are triggered by psychoactive substances .

The scientific interest in mind-altering drugs ( psychodysleptics ) has a tradition that goes back around a century. Many studies showed that the experiences triggered by some psychodysleptics (model psychoses) had certain similarities with acute psychotic attacks of a schizophrenic type; hence the name psychotomimetics . The degree of agreement is still controversial today.

On the other hand, the destabilizing effect on the psyche is successfully used to increase sensation and imagination in analytical psychotherapy.

There was a lot of discussion about the effects of LSD in the 1950s . The obstruction of research in this area by restrictive legislation around the world caused scientific interest to wane. However, at present, from around 1990 onwards, human-experimental research in the field of model psychoses, triggered by psychotomimetics, is experiencing a certain revival: also due to the development of apparatus, which allow ever more precise examination methods for ongoing chemical-physiological brain processes, for example computed tomography , Positron Emission Tomography (PET) and SPECT . Here, brain activities can be made visible and correlated with certain mental and emotional states or processes.

The question of whether a drug-induced state of consciousness can be a useful model for schizophrenic psychoses should be asked according to Gouzoulis et al. to be approached anew. The arguments currently put forward suggest that the experimentally generated psychosis is a useful model for acute schizophrenic psychoses (relapses), but not for the pathological entity "schizophrenia".

Biochemical aspects

In animal models, three classes of psychotropic drugs that act at distinct neurotransmitter systems that trigger psychosis-like symptoms: glutamate antagonists (eg. Phencyclidine ), serotonin - agonists (eg. LSD ) and dopamine agonists (eg. B. Amphetamines and Mescaline ). These three signal transduction pathways lead to DARPP-32, a triply phosphorylatable protein. DARPP-32 knock-out mice or animals mutated in DARPP-32 phosphorylation sites are significantly less affected by these three psychodysleptic groups than the unchanged animals. The mechanisms of action of these three groups of substances seem to act on a common molecular target structure.

See also

Individual evidence

  1. ↑ Claudio Naranjo , Santiago and Kensington: The journey to the self, psychotherapy with healing drugs, treatment protocols, Fischer Taschenbuchverlag, 1987, 880- ISBN 3-596-23381-X
  2. ↑ Hanscarl Leuner , Psychiatry Univ. Göttingen: Hallucinogens, psychological limit states in research and psychotherapy , Verlag Hans Huber, Bern, ISBN 3-456-80933-6
  3. ↑ Hans Bangen: History of the drug therapy of schizophrenia. Berlin 1992, ISBN 3-927408-82-4 . Page 10
  4. ↑ E. Gouzoulis-Mayfrank, L. Hermle, B. Thelen, H. Sass: History, rationale and potential of human experimental hallucinogenic drug research in psychiatry. . In: Pharmacopsychiatry . 31 Suppl 2, July 1998, pp. 63-68. doi : 10.1055 / s-2007-979348 . PMID 9754835 .
  5. ^ P. Svenningsson, ET. Tzavara, R. Carruthers, I. Rachleff, S. Wattler, M. Nehls, DL. McKinzie, AA. Fienberg u. a .: Diverse psychotomimetics act through a common signaling pathway. . In: Science . 302, No. 5649, November 2003, pp. 1412-1415. doi : 10.1126 / science.1089681 . PMID 14631045 .