Tritiated LSD Binding in Frontal Cortex in Schizophrenia

Earlier reports suggested that LSD binding to serotonin receptors in the frontal cortex is reduced in schizophrenia, indicating fewer receptors. However, this analysis of 13 schizophrenic brains compared to 8 control brains found no overall decrease in binding. Residual neuroleptic drugs in brain tissue, which are difficult to wash out, may have caused the earlier findings; chlorpromazine-treated rats showed reduced binding affinity consistent with this. In five patients likely neuroleptic-free for the year before death, LSD binding was significantly increased, though this requires replication in larger samples.

Study at a glance

Abstract

It has been reported that the binding of tritiated LSD (at 2 or 4 nm) to frontal cortex is reduced in schizophrenia, a finding that has been interpreted as a reduction in the number of serotonin receptors. The present study, however, reveals in a Scatchard analysis of tritiated LSD binding in frontal cortex in the brains of 13 schizophrenic patients that there was no decrease in binding by comparison with eight control brains. Quantities of neuroleptic remaining in the brain after death cannot be readily washed out and could have led to the previous report of reduced LSD binding. A decrease in affinity of LSD binding sites consistent with this possibility has been demonstrated in chlorpromazine-treated rats. In the brains of five patients who had probably been neuroleptic-free for the year before death, tritiated LSD binding was significantly increased. This result needs to be replicated in larger samples.