Journal of psychiatric research
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Borderline personality disorder (BPD) is a serious psychiatric disorder affecting about 1-2% of the general population. Key features of BPD are emotional instability, strong impulsivity, repeated self-injurious behavior (SIB) and dissociation. In the etiology of BPD and its predominant symptoms, genetic factors have been suggested. ⋯ However, in the female and in the male subsample, different SCN9A markers and individual haplotypes showed uncorrected p-values<0.05. In addition, p-values<0.05 were observed in the analysis of associations between SCN9A markers and dissociative symptoms. Although our results were largely negative, replication studies in an independent sample are warranted to follow up on the potential role of SCN9A gene variants in BPD and dissociative symptoms, paying special attention to a possible gender different etiology.
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Nocturnal awakenings are one of the most prevalent sleep disturbances in the general population. However, little is know about how its severity affects co-morbidity with mental disorders and organic diseases. ⋯ Nocturnal awakenings disrupt the sleep of about one third of the general population. Nocturnal awakenings are associated with a wide variety of organic diseases and psychiatric disorders that warrant appropriate treatment.
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Extracellular signal-regulated kinase (ERK) signal transduction pathway is widely implicated in multiple physiological processes. However, it remains to be determined whether ERK pathway plays roles in anxiety. Here we investigated the changes of phosphorylated ERK1/2 (pERK1/2) and c-Fos expression by immunostaining in the medial prefrontal cortex (mPFC) of anxious rats. ⋯ Inhibition of ERK phosphorylation blocked the anxiety-induced c-Fos expression. In the animal behavioral tests, the PD98059-treated anxious rats had a significant increase in the numbers of the open-arm entries, the time spent in the open-arms and the numbers of head-dipping in EPM test, and increase the inner locomotion in the open field test compared with the anxious rats. The results suggested that the ERK signal transduction pathway might play an important role in anxiety, and inhibition of the ERK pathway in the mPFC could produce anxiolysis effect.
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Clinical Trial
Dex/CRH-test response and sleep in depressed patients and healthy controls with and without vulnerability for affective disorders.
Sleep electroencephalographic (EEG) abnormalities and increased hypothalamo-pituitary-adrenal (HPA) axis activity are the most prominent neurobiological findings in depression and were suggested as potential biomarker for depression. In particular, increased rapid eye movement sleep (REM) density, deficit in slow wave sleep and excessive stress hormone response are associated with an unfavorable long-term outcome of depression. Recent studies indicate that the sleep and endocrine parameters are related to each other. ⋯ HRPs and patients with high disease vulnerability, indicated by an elevated REM density, seem to have a lower threshold until an actual disease process affecting the HPA axis translates into depression, and vice versa. To summarize, our findings provide further evidence that the HPA axis is involved in the sleep regulation in depression. These associations, however, are not unidimensional, but dependent on the kind of sleep parameters as well as on the selection of the subjects.
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Comparative Study
Pain perception in schizophrenia: no changes in diffuse noxious inhibitory controls (DNIC) but a lack of pain sensitization.
Pain is a dynamic phenomenon resulting from the activity of both excitatory (e.g. sensitization) and inhibitory endogenous modulation systems. Preliminary experimental studies have shown diminished pain sensitivity in schizophrenia patients. The objective of the study was to investigate the role of excitatory and inhibitory systems on pain perception in schizophrenia. ⋯ Diminished pain sensitivity in schizophrenia may be related to abnormal excitatory mechanisms, but not to DNIC. More studies are needed to better characterize the neurophysiological and neurochemical mechanisms involved in the lack of sensitization in schizophrenia.