Format

Send to

Choose Destination
Biol Psychiatry. 2011 Mar 1;69(5):399-406. doi: 10.1016/j.biopsych.2010.10.002. Epub 2010 Dec 3.

The 5-HT2A/1A agonist psilocybin disrupts modal object completion associated with visual hallucinations.

Author information

1
University Hospital of Psychiatry, Neuropsychopharmacology and Brain Imaging and Heffter Research Center, Lenggstrasse 31, Zurich, Switzerland. michael.kometer@bli.uzh.ch

Abstract

BACKGROUND:

Recent findings suggest that the serotonergic system and particularly the 5-HT2A/1A receptors are implicated in visual processing and possibly the pathophysiology of visual disturbances including hallucinations in schizophrenia and Parkinson's disease.

METHODS:

To investigate the role of 5-HT2A/1A receptors in visual processing the effect of the hallucinogenic 5-HT2A/1A agonist psilocybin (125 and 250 μg/kg vs. placebo) on the spatiotemporal dynamics of modal object completion was assessed in normal volunteers (n = 17) using visual evoked potential recordings in conjunction with topographic-mapping and source analysis. These effects were then considered in relation to the subjective intensity of psilocybin-induced visual hallucinations quantified by psychometric measurement.

RESULTS:

Psilocybin dose-dependently decreased the N170 and, in contrast, slightly enhanced the P1 component selectively over occipital electrode sites. The decrease of the N170 was most apparent during the processing of incomplete object figures. Moreover, during the time period of the N170, the overall reduction of the activation in the right extrastriate and posterior parietal areas correlated positively with the intensity of visual hallucinations.

CONCLUSIONS:

These results suggest a central role of the 5-HT2A/1A-receptors in the modulation of visual processing. Specifically, a reduced N170 component was identified as potentially reflecting a key process of 5-HT2A/1A receptor-mediated visual hallucinations and aberrant modal object completion potential.

PMID:
21126732
DOI:
10.1016/j.biopsych.2010.10.002
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science Icon for Zurich Open Access Repository and Archive
Loading ...
Support Center