Areas that show over-activity following tryptophan depletion in depression patients in remission — and thought to reflect a trait dysfunction — include emotion regulating circuitry involving the anterior cingulate, thalamus, ventral striatum and orbitofrontal cortex.
A brain imaging study by the NIH’s National Institute of Mental Health (NIMH) has found that an emotion-regulating brain circuit is overactive in people prone to depression – even when they are not depressed. Researchers discovered the abnormality in brains of those whose depressions relapsed when a key brain chemical messenger was experimentally reduced. Even when in remission, most subjects with a history of mood disorder experienced a temporary recurrence of symptoms when their brains were experimentally sapped of tryptophan, the chemical precursor of serotonin, the neurotransmitter that is boosted by antidepressants.
Neither a placebo procedure in patients nor tryptophan depletion in healthy volunteers triggered the mood and brain activity changes. Brain scans revealed that a key emotion-processing circuit was overactive only in patients in remission – whether or not they had re-experienced symptoms – and not in controls. Since the abnormal activity did not reflect mood state, the finding suggests that tryptophan depletion unmasks an inborn trait associated with depression.
Alexander Neumeister, M.D., Dennis Charney, M.D., Wayne Drevets, M.D., NIMH Mood and Anxiety Disorders Program, and colleagues, report on their positron emission tomography (PET) scan study in the August 2004 Archives of General Psychiatry.
Jules Asher | EurekAlert!
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