ObjectiveS100B is a neurotrophic factor that is involved in neuroplasticity. Neuroplasticity is disrupted in depression; however, treatment with antidepressants can restore neuroplasticity. S100B has previously been used as a biological marker for neuropathology and neuroplasticity; therefore, in this study, we compared serum S100B levels in depressive patients to those of normal controls. In addition, we compared the serum S100B levels of antidepressant responders to those of nonresponders.MethodsThirty five normal controls and 59 depressive patients were enrolled in this study. Depressive patients entered a 6 week clinical trial that included treatment with antidepressants. The serum S100B levels and clinical assessments, which included Hamilton depression rating scores, were measured at baseline and after 6 weeks of treatment with antidepressants. The difference in the serum S100B levels between depressive patients and normal controls and between antidepressant responders and nonresponders was then compared.ResultsThere were no significant differences in the serum S100B levels of normal controls and depressive patients. In addition, 30 of the depressive patients responded to antidepressant treatment while 29 did not. Finally, the responders had significantly higher baseline serum S100B levels than the nonresponders.ConclusionThe results of this study suggest that the baseline serum S100B level is associated with the subsequent response to antidepressants. In addition, the high baseline serum S100B level that was observed in depressive patients may enhance neuroplasticity, which results in a favorable therapeutic response to antidepressants.

The study aimed to investigate whether a combination of the P3-based Guilty Knowledge Test (GKT) and reality monitoring (RM) distinguished between individuals who are guilty, witnesses, or informed, and using both tests provided more accurate information than did the use of either measure alone. Participants consisted of 45 males that were randomly and evenly assigned to three groups (i.e., guilty, witness, and informed). The guilty group conducted a mock crime where they intentionally crashed their vehicle into another vehicle in a virtual environment (VE). As those in the witness group drove their own vehicles, they observed the guilty groups' vehicle crash into another vehicle. The informed group read an account and saw screenshots of the accident. All participants were instructed to insist that they were innocent. Subsequently, they performed the P3-based GKT and wrote an account of the accident for the RM analysis. A higher P3 amplitude corresponded to how well the participants recognized the presented stimulus, and a higher RM score corresponded to how well the participants reported vivid sensory information and how much less they reported uncertain information. Findings for the P3-based GKT indicated that the informed group showed lower P3 amplitude when presented with the probe stimulus than did the guilty and witness groups. Regarding the RM analysis, the informed group obtained higher RM scores on visual, temporal, and spatial details and lower scores on cognitive operations than the guilty and witness groups. Finally, discriminant analysis revealed that the combination of the P3-based GKT and RM more accurately distinguished between the three groups than the use of either measure alone. The findings suggest that RM may build upon a weakness of the P3-based GKT's. More specifically, it may build upon its susceptibility to the leakage of information about the crime, therefore helping protect innocent individuals who have information about a crime from being perceived as guilty.

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Changes in P300 amplitude were used as an indicator of reactivity to smoking-related stimuli in smokers. The amplitude of P300--a component of event-related brain potentials (ERPs) elicited by 10 smoking-related (craving), 10 antismoking (aversive) and 10 neutral stimuli-- was recorded in smokers (n=10) and nonsmokers (n=10). Electroencephalography (EEG) data were obtained by the Laxtha EEG-monitoring device in the EEG recording room, and were recorded at F3, F4, C3, and C4. Three-way repeated-measures analysis of variance (ANOVA) was computed on the P300 amplitudes. The factors were group (smokers, nonsmokers), stimulus (craving, aversive, neutral), and electrode location (F3, F4, C3, and C4). The main effects of stimulus were significant, but the group effects did not show significant interactions with other factors. An interesting observation was the similarity between P300 waveforms for craving and aversive stimuli in smokers. These findings could indicate that the antismoking-related response is similar to the smoking-related one.

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