Yale School of Medicine researchers published
a report this month in the Archives of General Psychiatry that highlights
the interplay of two brain signaling systems, glutamate and dopamine,
in psychosis and cognitive function.
The study helps resolve a long-standing research debate between the “dopamine
hypothesis” and the “glutamate hypothesis” or “PCP
Model,” said John Krystal, M.D., professor, deputy chair for research
in the Department of Psychiatry, and lead author of the study.
“ Both
systems appear to be involved,” he said.
The first theory suggests that dopamine neurons are hyperactive in persons
with schizophrenia and that effects of the dopamine-releasing drug, amphetamine,
can mimic aspects of the illness. The second theory maintains that certain
schizophrenia-related deficits in the function of glutamate, the dominant
stimulatory transmitter, could be reproduced in healthy people by the
administration of drugs such as ketamine, which block the NMDA subtype
of glutamate receptors.
The study included 41 healthy subjects who were given amphetamine, ketamine
and then saline, in varying sequence. The researchers found the transient
psychotic state produced by each drug was similar but not identical and
that ketamine produced a more “complete” schizophrenia-like
state than amphetamine.
They also found that cognitive impairments produced
by ketamine, specifically working memory, were reduced by the administration
of amphetamine.
“ This study lends support to the hypothesis that drugs
that facilitate the function of particular dopamine receptors might
play
a role in treating
cognitive impairments associated with schizophrenia,” Krystal
said.
The study was conducted at the VA Connecticut Healthcare
System with support from the National Alliance for Research on Schizophrenia
and
Affective Disorders, the National Institute of Mental Health and the
Department of Veterans Affairs.
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