Inhibitory neurotransmission in frontostriatal circuitry: implications for psychomotor and vegetative symptoms in depressive episodes
Abstract
Background: Gamma-aminobutyric acid (GABA) dysfunction has been implicated in depression, although research findings remain inconsistent. This may indicate that distinct biological mechanisms underlie different symptom profiles in depressive episodes. Altered GABA function might be especially relevant in cases characterised by psychomotor retardation and vegetative symptoms, which are prominent in melancholia. This study aimed to investigate if such melancholic features are related to GABA levels or GABAA-receptor availability.
Methods: This was a secondary analysis of data obtained from a randomised controlled trial. Forty-two patients with either bipolar or unipolar depression were assessed before and after a course of repetitive transcranial magnetic stimulation. GABA and glutamate levels in the dorsal anterior cingulate cortex (dACC) were measured using a [1H] magnetic resonance spectroscopy MEGA-PRESS sequence. A subset of 28 patients underwent [11C]flumazenil positron emission tomography (PET) to evaluate GABAA-receptor availability in the dACC, basal ganglia, and hypothalamus. Psychomotor retardation was assessed with the expression subscale of the Clinical Assessment Interview for Negative Symptoms. Sleep disturbances were evaluated using components of the Pittsburgh Sleep Quality Index, while appetite loss was measured using an item from the Montgomery-Åsberg Depression Rating Scale - self-rated. The scores were standardised and combined to create composite measures…
How strong is the evidence?
Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 28 participants or records.
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