Abstract
Objectives: To first explore the role of plasma vascular endothelial growth factor (VEGF) concentrations in ketamine's antianhedonic effects, focusing on Chinese patients with treatment-refractory depression (TRD).Methods: Seventy-eight patients with treatment-refractory major depressive disorder (MDD) or bipolar disorder (BD) were treated with six ketamine infusions (0.5 mg/kg). Levels of anhedonia were measured using the Montgomery–Åsberg Depression Rating Scale (MADRS) anhedonia item at baseline, day 13 and 26. Plasma VEGF concentrations were examined at the same time points as the MADRS.Results: Despite a significant reduction in anhedonia symptoms in individuals with treatment-refractory MDD (n = 59) or BD (n = 19) after they received repeated-dose ketamine infusions (p < 0.05), no significant changes in plasma VEGF concentrations were found at day 13 when compared to baseline (p > 0.05). The alteration of plasma VEGF concentrations did not differ between antianhedonic responders and non-responders at days 13 and 26 (all ps > 0.05). Additionally, no significant correlations were observed between the antianhedonic response to ketamine and plasma VEGF concentrations (all ps > 0.05).Conclusion: This preliminary study suggests that the antianhedonic effects of ketamine are not mediated by VEGF.
Highlights
Anhedonia, a reduced capacity for pleasure, is regarded as one of the typical characteristics of major depressive disorder (MDD) and bipolar depression (BD) [1] and appears to occur irrespective of other depressive symptoms [2, 3]
A single ketamine infusion could rapidly ameliorate anhedonia symptoms in individuals suffering from treatmentrefractory BD; the reduction in anhedonia symptoms occurred within 40 min and lasted up to 14 days [10]
We report the relationship of plasma vascular endothelial growth factor (VEGF) concentrations and antianhedonic effects of subanaesthetic doses of ketamine, focusing on individuals suffering from treatment-refractory MDD or BD
Summary
A reduced capacity for pleasure, is regarded as one of the typical characteristics of major depressive disorder (MDD) and bipolar depression (BD) [1] and appears to occur irrespective of other depressive symptoms [2, 3]. Anhedonia is a robust predictor of poor outcomes [4] and suicidal ideation independent of neurocognitive dysfunction and affective symptoms [5], suggesting that it appears to be an independent somatic domain in mood disorders [3]. VEGF and Antianhedonic Effects of Ketamine from treatment-refractory depression (TRD) treated with conventional pharmacotherapy [6]. Especially those with TRD, frequently endorse disturbance in reward capacity, providing the impetus for exploring novel agents and treatment approaches [7, 8]. In addition to the rapid effect on depressive symptoms, ketamine has rapid and robust effects on anhedonia symptoms [1, 9, 10] and suicidal ideation [11,12,13] in treatment-refractory BD and MDD. Ketamine’s antianhedonic effects occur independently of the reduction in depressive symptoms [10]
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