Serum nitric oxide levels are depleted in depressed patients treated with electroconvulsive therapy.

BACKGROUND: Nitric oxide (NO) is an endogenous substance which has several endocrine functions and may act as neurotransmitter in the brain. High levels of NO may provoke nitrosative stress. AIM: It was aimed to examine serum levels of NO in patients with depressive episodes who were treated with electroconvulsive therapy (ECT) in this study. METHODS: The design was a case-control, follow-up study. Patients with depressive episodes (n = 23) and a healthy control group (n = 21) were enrolled. Three serum samples were obtained from the patient group (before ECT, after first and seventh sessions). NO, nitrite, and nitrate levels were examined. STATISTICAL ANALYSIS: Differences between groups were examined with t-test or Mann-Whitney U-test. Longitudinal data were evaluated with Panel Regression Analysis and Kruskal-Wallis Test. RESULTS: Serum levels of NO and nitrite decreased significantly after the seventh session of ECT administration compared to the baseline and first session. Nitrate levels did not differ between the assessments. CONCLUSIONS: Reduction of the serum NO and nitrite levels might be a contributing factor for hypertension during the sessions. These findings are reflect the circulating NO levels. Further studies may dissect NO physiology in the brain in mental disorders and potential external effects.

Electroconvulsive Therapy and Extracellular Matrix Glycoproteins in Patients with Depressive Episodes.

Background: The brain extracellular matrix (ECM) is composed of glycoproteins deriving from the cell membrane and joining into nets called perineuronal nets (PNNs). The ECM glycoproteins limit neuroplasticity, cell proliferation, and differentiation. Electroconvulsive therapy (ECT) is provided by electrical currents that may alter several cascades and biophysical effects. ECM conformation might be influenced by the effects of ECT. Methods: Patients with depressive disorders (n = 23) and healthy control subjects (n = 21) were enrolled. Serum levels of the ECM glycoproteins versican, brevican, neurocan, phosphocan and tenascin C were measured with enzyme-linked immunosorbent assay. Serum samples were collected from the patients in the patient group at 3 time points: before ECT, 30 min after the first session, and 30 min after the seventh session. Results: There was a significant difference in tenascin C levels (P = .001) between the groups. No other significant difference was observed. Serum levels of the measured ECM glycoproteins and prolidase activity did not differ in the depression group after the administration of ECT. Conclusions: Our results did not support the claim suggesting a possible mechanism for modulation of ECM glycoproteins by ECT. Serum levels may not necessarily reflect conformational changes in the ECM. Further studies are needed to investigate the effects of ECT on ECM glycoproteins. Modulation of the ECM may provide a new window suggesting improvement in treatments.