Brain areas associated with resilience to depression in high-risk young women.

Previous structural brain-imaging studies in first-degree relatives of depressed patients showed alterations that are generally accepted as vulnerability markers for depression. However, only half of the relatives had depression at follow-up, while the other half did not. The aim of this study was to identify the brain areas associated with resilience to depression in high-risk subjects with familial depression. We recruited 59 young women with a history of depressed mothers. Twenty-nine of them (high-risk group [HRG]) had no depression history, while 30 (depressive group) had at least 1 depressive episode in adolescence. The brain structures of the groups were compared through voxel-based morphometry and analysis of cortical thickness. Individual amygdala nuclei and hippocampal subfield volumes were measured. The analysis showed larger amygdala volume, thicker subcallosal cortex and bilateral insula in the women in the HRG compared with those in the depressive group. In addition, we detected more gray matter in the left temporal pole in the HRG. The larger gray matter volume and increased cortical thickness in the key hub regions of the salience network (amygdala and insula) and structurally connected regions in the limbic network (subcallosal area and temporal pole) might prevent women in the HRG from converting to depression.

Effects of olanzapine on auditory P300 in schizophrenia.

Reduced auditory P300 amplitude generally has been considered to be a trait marker of schizophrenia, independent of antipsychotic treatment and clinical symptoms. However, several seemingly well-conducted studies have found P300 amplitude to be a state marker correlated with clinical symptoms. Recent research on atypical antipsychotics indicate that these medications may alter P300 amplitude as well as having beneficial clinical effects. The objective of the present study was to further elucidate the effects of schizophrenia, symptom severity, and medication status on the P300. The baseline auditory P300 was assessed in unmedicated schizophrenic patients who then were treated with olanzapine for 6 weeks and reassessed. Healthy control subjects were assessed at baseline and again at 6 weeks. Compared to healthy controls, the unmedicated patients' P300s were attenuated and delayed prior to treatment. Subsequent antipsychotic treatment increased the patients' P300 amplitudes without affecting latency. Frontal P300 amplitude was normalized, but parietal P300 amplitude remained below that of healthy controls. Although olanzapine was effective in reducing the patients' symptoms, there were no correlations between symptoms and P300 amplitude or latency either before or after treatment. The results of the present study lend support to the view that P300 amplitude behaves as a trait marker. No evidence is found of a P300 clinical state marker.

Reduced reward-related probability learning in schizophrenia patients.

Although it is known that individuals with schizophrenia demonstrate marked impairment in reinforcement learning, the details of this impairment are not known. The aim of this study was to test the hypothesis that reward-related probability learning is altered in schizophrenia patients. Twenty-five clinically stable schizophrenia patients and 25 age- and gender-matched controls participated in the study. A simple gambling paradigm was used in which five different cues were associated with different reward probabilities (50%, 67%, and 100%). Participants were asked to make their best guess about the reward probability of each cue. Compared with controls, patients had significant impairment in learning contingencies on the basis of reward-related feedback. The correlation analyses revealed that the impairment of patients partially correlated with the severity of negative symptoms as measured on the Positive and Negative Syndrome Scale but that it was not related to antipsychotic dose. In conclusion, the present study showed that the schizophrenia patients had impaired reward-based learning and that this was independent from their medication status.

The effects of long-term sleep deprivation on the long-term potentiation in the dentate gyrus and brain oxidation status in rats.

Some evidence suggests that sleep deprivation might impair synaptic plasticity and produce oxidative stress in the hippocampus. However it is not clear whether impairment of long-term potentiation depends on the oxidative stress evoked by sleep deprivation protocol. In this study we aimed to investigate the effects of a 21-day sleep deprivation period on long-term plasticity taking into account the stressful effect of sleep deprivation. Sleep deprivation was carried out using the multiple platforms method on adult male Wistar rats. Long-term potentiation was studied in the medial perforant pathway-dentate gyrus synapses. Elevated T test was applied, and blood corticosterone levels were measured. Lipid peroxidation products in whole brain and hippocampus were determined. No significant difference was found between the sleep deprived, pedestal and cage control groups at the end of the 21-day period when corticosterone levels were compared. The results of the elevated T test indicated that sleep deprivation did not change the anxiety-like behavior of the animals. When compared with cage or pedestal control groups, sleep deprived rats displayed elevated malondialdehyde levels, and decreased superoxide dismutase and glutathione peroxidase activities together with impaired long-term potentiation maintenance. It can be argued that 21-day SD may impair the maintenance of long-term potentiation evoked in the dentate gyrus, and the balance between oxidant and antioxidant defenses of the hippocampus.