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WESTPORT, Aug 15 (Reuters Health) - Patients with major depression have significantly fewer serotonin transporter (5-HTT) binding sites in the prefrontal cortex than nondepressed patients, researchers report in the August issue of Archives of General Psychiatry.
Dr. J. John Mann, of the New York State Psychiatric Institute in New York City, and colleagues examined postmortem brain samples from 82 people who had committed suicide and 138 nonsuicide controls. The lifetime major depression status was known for 160 of the subjects, where 53 had a history and 107 had no history.
The 220 samples were genotyped for a polymorphism in the 5-HTT gene that had been shown to affect expression of the transporter in cultured cells. In addition, 159 of the samples were quantitatively tested for serotonin binding to 5-HTT in the prefrontal cortex.
Compared with nonsuicides, suicidal patients had reduced binding to 5-HTT in the orbital or ventral prefrontal cortex, which "may reflect reduced serotonin input to that brain region, underlying the predisposition to act on suicidal thoughts," the researchers suggest.
Patients with major depression had reduced binding throughout the prefrontal cortex compared with those without depression, which "may reflect a widespread impairment of serotonergic function consistent with the range of psychopathologic features in major depression," according to the report.
The authors determined that the 5-HTT polymorphism was associated with major depression. However, it was not associated with suicide, and it did not correlate with binding to 5-HTT, even after the researchers corrected for a history of alcoholism, substance abuse, and pathological aggression.
Previous studies had already shown fewer serotonin transporter sites in platelets and the brain stem in depressed patients, Dr. Mann told Reuters Health. "This is the first study of the prefrontal cortex, which is obviously more relevant to the biology of depression than the platelet," he said. "It kind of fits with the idea that there's not enough serotonin around." He noted that reduced binding could be compensating for a lack of serotonin itself, an idea his group is testing.
He also suggested that imaging could potentially be used to detect the number of serotonin transporters in patients to diagnose depression.
Dr. J. John Mann, of the New York State Psychiatric Institute in New York City, and colleagues examined postmortem brain samples from 82 people who had committed suicide and 138 nonsuicide controls. The lifetime major depression status was known for 160 of the subjects, where 53 had a history and 107 had no history.
The 220 samples were genotyped for a polymorphism in the 5-HTT gene that had been shown to affect expression of the transporter in cultured cells. In addition, 159 of the samples were quantitatively tested for serotonin binding to 5-HTT in the prefrontal cortex.
Compared with nonsuicides, suicidal patients had reduced binding to 5-HTT in the orbital or ventral prefrontal cortex, which "may reflect reduced serotonin input to that brain region, underlying the predisposition to act on suicidal thoughts," the researchers suggest.
Patients with major depression had reduced binding throughout the prefrontal cortex compared with those without depression, which "may reflect a widespread impairment of serotonergic function consistent with the range of psychopathologic features in major depression," according to the report.
The authors determined that the 5-HTT polymorphism was associated with major depression. However, it was not associated with suicide, and it did not correlate with binding to 5-HTT, even after the researchers corrected for a history of alcoholism, substance abuse, and pathological aggression.
Previous studies had already shown fewer serotonin transporter sites in platelets and the brain stem in depressed patients, Dr. Mann told Reuters Health. "This is the first study of the prefrontal cortex, which is obviously more relevant to the biology of depression than the platelet," he said. "It kind of fits with the idea that there's not enough serotonin around." He noted that reduced binding could be compensating for a lack of serotonin itself, an idea his group is testing.
He also suggested that imaging could potentially be used to detect the number of serotonin transporters in patients to diagnose depression.
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