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BACKGROUND: Acute tryptophan depletion lowers brain serotonin synthesis and results in a transient, but striking, clinical relapse in recovered depressed patients. AIMS: To identify brain regions which change their activity as an acute depressive relapse evolves and to determine how pathological mood might modulate neural activity during a cognitive task. METHOD: We used H2(15)O positron-emission tomography (PET) to study eight recovered depressed men after tryptophan depletion and after a control procedure. During both PET scan sessions, subjects performed a paced verbal fluency task which alternated with a control verbal repetition task. RESULTS: Increasing levels of depression after tryptophan depletion were associated with diminished neural activity in the ventral anterior cingulate, orbitofrontal cortex and caudate nucleus regions. In addition, depressive relapse attenuated cognitive task-related activation in the anterior cingulate cortex. CONCLUSIONS: Our data indicate that changes in neural activity in distinct brain regions mediate the clinical phenomena of depression and depression-related cognitive impairment following acute tryptophan depletion. These changes could be associated with the widespread distribution of serotonin neurons in brain pathways associated with the expression of affect and cognitive performance.

Type

Journal article

Journal

Br J Psychiatry

Publication Date

06/1999

Volume

174

Pages

525 - 529

Keywords

Adult, Blood Flow Velocity, Brain Diseases, Cerebrovascular Circulation, Cognition Disorders, Depressive Disorder, Humans, Male, Middle Aged, Psychological Tests, Recurrence, Serotonin, Tomography, Emission-Computed, Tryptophan