Brain-Derived Neurotrophic Factor Response in Vulnerable and Resilient Genetic Lines in the Chick Anxiety-Depression Model.

Brain-derived neurotrophic factor response in vulnerable and resilient genetic lines in the chick anxiety-depression model.

Filed under: Depression Treatment

Behav Brain Res. 2013 Feb 5;
Loria MJ, White SW, Robbins SA, Salmeto AL, Hymel KA, Murthy SN, Manda P, Sufka KJ

Altered BDNF-mediated synaptogenesis is a major contributor to stress-vulnerability and depression. This study sought to determine patterns of hippocampal BDNF expression in stress-vulnerable and -resilient strains in the chick anxiety-depression model. Socially raised Black Australorp and Production Red strains were tested at 5-6 days post hatch under either 30, 60, 90, or 120min of social separation stress; chicks tested with 2 social companions for 120min served as a controls. Distress vocalizations were recorded throughout the test session and latency to behavioral despair calculated. Following tests, bilateral hippocampal sections were harvested and analyzed via ELISA for BDNF levels. Black Australorps had shorter latencies to behavioral despair than Production Reds reflecting greater stress vulnerability. No differences were detected in BDNF levels between a No-Test and Social group within or between strains. The stress resilient Production Reds showed stable BDNF levels across the isolation test period whereas the vulnerable Black Australorps showed an increase in hippocampal BDNF levels that peaked at 90min and declined thereafter. These findings fit well with the notion that strain-dependent stress-vulnerability reflects, in part, poor homeostatic mechanisms controlling synaptogenesis.
HubMed – depression

Empathy and social problem solving in alcohol dependence, mood disorders and selected personality disorders.

Filed under: Depression Treatment

Neurosci Biobehav Rev. 2013 Feb 5;
Thoma P, Friedmann C, Suchan B

Altered empathic responding in social interactions in concert with a reduced capacity to come up with effective solutions for interpersonal problems have been discussed as relevant factors contributing to the development and maintenance of psychiatric disorders. The aim of the current work was to review and evaluate 30 years of empirical evidence of impaired empathy and social problem solving skills in alcohol dependence, mood disorders and selected personality disorders (borderline, narcissistic, antisocial personality disorders/psychopathy), which have until now received considerably less attention than schizophrenia or autism in this realm. Overall, there is tentative evidence for dissociations of cognitive (e.g. borderline personality disorder) vs. emotional (e.g. depression, narcissism, psychopathy) empathy dysfunction in some of these disorders. However, inconsistencies in the definition of relevant concepts and their measurement, scarce neuroimaging data and rare consideration of comorbidities limit the interpretation of findings. Similarly, although impaired social problem solving appears to accompany all of these disorders, the concept has not been well integrated with empathy or other cognitive dysfunctions as yet.
HubMed – depression

Acanthopanax senticosus exerts neuroprotective effects through HO-1 signaling in hippocampal and microglial cells.

Filed under: Depression Treatment

Environ Toxicol Pharmacol. 2013 Jan 14; 35(2): 335-346
Jin ML, Park SY, Kim YH, Park G, Lee SJ

Extracts of Acanthopanax senticosus, a traditional herb commonly found in Northeastern Asia, are used for treating neurodegenerative disorders such as ischemia and depression. However, the mechanisms of its neuroinflammatory and cytoprotective effects have not been investigated. We examined the mechanism of A. senticosus activity in anti-neuroinflammatory and neuroprotective processes. HO-1 is an inducible enzyme present in most cell lines. ASE increased HO-1 expression, which reduced LPS-induced nitric oxide/ROS production in BV2 cells. Moreover, the induction of HO-1 expression protected cells against glutamate-induced neuronal cell death. Activation of the p38-CREB pathway and translocation of Nrf2 are strongly involved in ASE-induced HO-1 expression. Our results showed that ASE-induced HO-1 expression through the p38-CREB pathway plays an important role in the generation of anti-neuroinflammatory and neuroprotective responses. ASE also increases the translocation of Nrf2 to regulate HO-1 expression. Furthermore, our results indicate that ASE serves as a potential therapeutic agent for neuronal disorders.
HubMed – depression

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