Neuroscience_topics
20.4K views | +0 today
Follow
Neuroscience_topics
Neuroscience: CNS disease, pain, brain research, ion channels, synaptic transmission, channelopathies, neuronal network
Your new post is loading...
Your new post is loading...
Scooped by Julien Hering, PhD
Scoop.it!

[Review] Epigenetic Mechanisms of Depression and Antidepressant Action

[Review] Epigenetic Mechanisms of Depression and Antidepressant Action | Neuroscience_topics | Scoop.it

[Abstract] Epigenetic mechanisms, which control chromatin structure and function, mediate changes in gene expression that occur in response to diverse stimuli. Recent research has established that environmental events and behavioral experience induce epigenetic changes at particular gene loci and that these changes help shape neuronal plasticity and function and hence behavior. Some of these changes can be stable and can even persist for a lifetime. Increasing evidence supports the hypothesis that aberrations in chromatin remodeling and subsequent effects on gene expression within limbic brain regions contribute to the pathogenesis of depression and other stress-related disorders such as post-traumatic stress disorder and other anxiety syndromes. Likewise, the gradually developing but persistent therapeutic effects of antidepressant medications may be achieved in part via epigenetic mechanisms. This review discusses recent advances in our understanding of the epigenetic regulation of stress-related disorders and focuses on three distinct aspects of stress-induced epigenetic pathology: the effects of stress and antidepressant treatment during adulthood, the lifelong effects of early-life stress on subsequent stress vulnerability, and the possible transgenerational transmission of stress-induced abnormalities. - by Vialou V et al., Annual Review of Pharmacology and Toxicology, 53(1):59

more...
No comment yet.
Scooped by Julien Hering, PhD
Scoop.it!

Are We Getting Closer to Valid Translational Models for Major Depression?

[Review] Advances in characterizing the neuropathology and functional dysconnectivity of depression and promising trials with emerging circuit-targeted and fast-onset therapeutics are providing unprecedented opportunities to gain deeper insight into the neurobiology of this devastating and pervasive disorder. Because of practical and ethical limitations to dissecting these mechanisms in humans, continued progress will critically depend on our ability to emulate aspects of depressive symptomatology and treatment response in nonhuman organisms. Although various experimental models are currently available, they often draw skepticism from both clinicians and basic research scientists. We review recent progress and highlight some of the best leads to diversify and improve discovery end points for preclinical depression research. (...) by Berton O. et al.Science Vol. 338 no. 6103 pp. 75-79, 5 October 2012

more...
No comment yet.
Scooped by Julien Hering, PhD
Scoop.it!

Synaptic Dysfunction in Depression: Potential Therapeutic Targets

[Review] Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response. by Dunam RS & Aghajanian GKScience 5 October 2012: Vol. 338 no. 6103 pp. 68-72

more...
No comment yet.