Cortical thickening in remitters compared to non-remitters with major depressive disorder following 8-week antidepressant treatment.

OBJECTIVE: Little is known about the relationship between antidepressant treatment outcomes and underlying neurobiological mechanisms in patients with major depressive disorder (MDD). In this prospective study, we aimed to investigate how cortical thickness and subcortical volumes differed between remitter and non-remitter patients with MDD. METHODS: Fifty-eight patients with MDD with a score of at least 17 on the 17-item Hamilton Depression Rating Scale and free of medication for at least 2 months and 41 healthy controls underwent structural magnetic resonance imaging. At the baseline, patients with MDD started on either selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, or vortioxetine. After 8-week antidepressant treatment, patients with MDD were scanned using the same MRI protocol. Structural images were analyzed using the FreeSurfer software package (version 6.0). RESULTS: Longitudinal analyses showed remitter patients with MDD had significantly greater right cerebral cortex thickening in six significant clusters, including superior temporal cortex, precuneus, rostral middle frontal cortex, pars opercularis (although the cluster extends into the insula), inferior parietal cortex, and supramarginal cortex than in non-remitter patients with MDD. CONCLUSION: Our results suggest that distinct antidepressant treatment-related structural alterations in brain regions implicated in cognition, emotion regulation, and rumination might be associated with treatment outcome.

Short-term thyroxine administration leads to lipid peroxidation in renal and testicular tissues of rats with hypothyroidism.

Thyroid dysfunction brings about pathological changes in different organs of the body. The aim of the present study was to examine how experimental hypothyroidism and additional short-term high-dose thyroxine administration (one-week) affected lipid peroxidation in renal and testicular tissues of rats. The study was carried out on 30 male Spraque-Dawley rats. The experimental animals were divided into 3 groups as control, hypothyroidism and hypothyroidism + thyroxine administration. Both malondialdehyde (MDA) and glutathione (GSH) levels were lower in renal and testicular tissues of the hypothyroidism group than the control and hypothyroidism + thyroxine administration groups and the levels in hypothyroidism + thyroxine administration group were higher than those in the control and hypothyroidism groups (p < 0.001). Results of the study demonstrate that hypothyroidism reduced oxidant stress in kidney and testis tissues, but short-term, high-dose thyroxine administration in addition to hypothyroidism increased oxidant stress in the same tissues of rats.

The effect of estradiol and progesterone application on leptin concentration in ovariectomized rats.

The aim of the present study was to investigate the effects of estradiol and progesterone application on leptin secretion in ovariectomised rats. The study included 30 adult female Sprague-Dawley rats. Rats were divided into three groups as follows: Group 1; Sham ovariectomy group (n=10), Group 2; Ovariectomy group (n=10), Group 3; Ovariectomized and estradiol propionate (450 microg/kg rat) and medroxyprogesterone acetate (15 mg/kg rat) supplemented group (n=10). One week after ovariectomy, rats in Group 3 were injected estradiol and progesterone for 4 weeks. Twenty-four hours after the last injection, rats were decapitated and blood samples were collected for leptin analysis. Serum leptin levels in Group 2 were found significantly higher than those in Groups 1 and 3 (p<0.01), while those in Group 3 were significantly lower when compared to Group 1 (p<0.0 1). The findings of the present study have shown that ovariectomy led to a significant increase in leptin levels. However, administration of estradiol and progesterone in combination following ovariectomy inhibites increases of leptin levels.

The effect of thyroxine administration on lipid peroxidation in different tissues of rats with hypothyroidism.

Thyroid dysfunctions bring about pathological changes in different organs of the body. Findings obtained from in vivo and in vitro studies point out that thyroid hormones have a strong impact on oxidative stress. The present study was conducted to demonstrate how high-dose thyroxin administration for one week affected oxidative damage formed in experimental hypothyroidism. The study was carried out with 30 Spraque-Dawley species male rats. The experimental animals were divided into 3 groups (Group 1, control; Group 2, hypothyroidism; Group 3, hypothyroidism + thyroxine administration). Malondialdehyde (MDA) and glutathione (GSH) levels were determined in cerebral, hepatic and cardiac tissues after the experimental period. MDA and GSH levels in cerebral, hepatic and cardiac tissues of hypothyroidism + thyroxine supplemented group were higher than those in the control and hypothyroidism groups (p<0.001). The same parameters were higher in the control group than those in the hypothyroidism group (p<0.001). The results of the present study show that hypothyroidism reduced the oxidative damage in cerebral, hepatic and cardiac tissues of rats. However, high-dose thyroxine administration in addition to induced hypothyroidism increased oxidative damage in the same tissues and that this damage could not be prevented despite the increase in the antioxidant system activity.