Altered consciousness states and endogenous psychoses: a common molecular pathway?

Interest in the role of indolamines in the pathogenesis of psychoses has been renewed in recent years by the development of atypical antipsychotic drugs such as clozapine, olanzapine, and risperidone, which act on serotonin receptors. Discovery of the hallucinogenic compounds called methylated indolealkyalamines (MIAs) (e.g. N,N-dimethylserotonin, or bufotenin, and N,N-dimethyltryptamine, or DMT) led proponents of the transmethylation hypothesis of schizophrenia to theorize that through some inborn error of metabolism, serotonin or tryptamine might undergo the addition of extra methyl radicals, thereby forming MIAs with hallucinogenic properties. Various studies have attempted to detect the excretion of MIAs, especially DMT, in the body fluids of psychotic patients and normal controls. Some of these studies have demonstrated elevated MIA concentrations in psychotic patients, including those with schizophrenia, compared with normal persons, and others have not. A number of variables may account for these contradictory findings. The mechanism whereby the beverage ayahuasca, which is used in certain cure and divination rituals in the Amazon Basin, exerts its hallucinogenic effects may serve as a model to explain the mechanism underlying hallucinogenic symptoms in schizophrenia and may lend support to the transmethylation hypothesis. Certain studies suggest that specific perceptual disturbances manifested by schizophrenic patients could contribute to progressive deterioration and negative symptomatology. All these findings point to the need for further study of the neurophysiology of MIAs and their pathogenetic role in endogenous psychoses.

Catecholamine changes in patients with depression under the action of high-intensity light. / Zminy katekholaminiv u khvorykh z depresiieiu pid diieiu svitla pidvyshchenoï intensyvnosti.

Preponderance in depression of the melancholy affect was characterized by a drop in the level of norepinephrine (NE) and rise in epinephrine (E). Exposure to light was associated with fall in E, with no change recordable in NE. In anxious depression, following light therapy, high levels of excretion of both catecholamines tended to return to normal. Ligh was found to cause opposite changes in the quantitative measures depending upon the initial value for the E:NE ratio (above or below control).

[Melatonin excretion in patients with depression under the action of light of increased intensity]. / Ekskretsiia melatonina u bol'nykh depressiei pri deistvii sveta povyshennoi intensivnosti.

The effects of 1 and 10 bright light exposures (2600-8000 lux) on melatonin excretion in patients with melancholic and anxious depressions were examined. Before treatment the increased basic levels of melatonin excretion were observed in patients with anxious depression. Melatonin excretion had been gradually normalized after 1 and 10 sessions of light therapy. The basic melatonin excretion in melancholic depressed patients was low and hadn't been changed after light therapy. Long term effects of light therapy depend upon the initial levels of melatonin excretion: low pretreatment levels increased and high pretreatment levels decreased after the therapy. The authors proposed that bright light exposures stimulated the restoration of adaptive function of pineal gland in depressed patients.

The effect of electric acupuncture treatment on urinary MHPG-sulphate excretion in unmedicated schizophrenics.

The daily urinary excretion of 3-methoxy-4-hydroxyphenylglycol sulphate (MHPG-SO4) was determined before and during the course of electric acupuncture treatment (EAT) in eight unmedicated schizophrenic patients. The mean excretion of MHPG-SO4 before treatment was 1439 +/- 74 micrograms/24 hr. EAT was administered once daily and continued for two weeks. The urinary MHPG-SO4 excretion steadily increased during the course of EAT. The mean values obtained during the first and second weeks of treatment were 1712 +/- 108 micrograms/24 hr and 1920 +/- 81 micrograms/24 hr respectively, each being significantly higher than the mean value obtained before EAT.