Possible mechanisms of panic attack and schizophrenia via APUD system.
K Fukuda
Medical Hypotheses February 2002 DOI: 10.1054/mehy.2001.1473 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Key points | The author postulates that psilocybin poisoning produces a biphasic reaction with a schizophrenic phase and a panic attack-like phase separated by several hours, possibly reflecting accumulation between gut and brain. The author argues that APUD cells, including foregut argyrophil cells, lung neuroepithelial bodies, and brainstem raphe nuclei, are relevant to mental disorders, and proposes that schizophrenia might arise from massive APUD cell destruction while paroxysmal release of 5-HT, peptides, and panneuroendocrine markers from neuroepithelial bodies might cause panic attacks. |
Abstract
Psilocybin poisoning produces biphasic reactions composed of a schizophrenic phase and a panic attack-like phase. There is a time lag of several hours between phases, which may be considered an accumulation time in certain sites between the gut and the brain. So far as 5-hydroxytryptamine (5-HT) congeners are concerned, no sites are to be found except the amine precursor uptake and decarboxylation (APUD) system. It is postulated that argyrophil cells (AC) in the foregut, neuroepithelial bodies (NEB) in the lung, and raphe nuclei (RN) in the brainstem axis are relevant to mental disorders. Schizophrenia might be due to the massive destruction of APUD cells, and the paroxysmal release of 5-HT with peptides and panneuroendocrine markers from NEB might be the cause of panic attack.