Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 4 • August 2012


We hope to explain the universe in a single, simple formula that you can wear on your T-shirt.

— Leon Lederman, in “Quark City” by
Richard Wolkomir, Omni Feb. 1984

(D&S: Mmmmm. That sounds good, and maybe the formula could become the basis of a new bubble on the stock market.)

Increased Expression of Brain-Derived Neurotrophic Factor (BDNF) Famously Increases Neurogenesis in the Hippocampus and Improves Cognition

But, New Report Finds That Increased Expression of BDNF Under Stressful Conditions Has Opposite Effects in Amygdala and Hippocampus

It might have seemed (for a little while, anyway) that increasing the expression of the neurotrophin BDNF might be an unalloyed great idea, as it was shown to enhance cognition by inducing neurogenesis when its expression was increased in the hippocampus. Now, new results1 show that things are not that simple (but then they rarely are).

On the basis of earlier studies, chronic administration of antidepressants were found to prevent stress-induced decrease in the level of BDNF and the increase of dendritic atrophy in the hippocampus. From this, the “neurotrophic hypothesis” of depression developed, that attributed depression to decreased neurotrophic support in the hippocampus and that restoring the neurotrophic support (such as by increasing BDNF levels) in that area of the brain would correct the symptoms of depression.1 The results of the new paper1 found, though, that chronic immobilization stress in eight week old adult male Wistar rats reduced BDNF expression in the CA3 area of the hippocampus but INCREASED the expression of BDNF in the BLA (basolateral amygdala), a different area of the brain that is particularly involved in emotional responses to stress, such as anxiety and fear. Under the conditions of chronic immobilization stress (CIS), there is dendritic atrophy in CA3 pyramidal neurons of the rodent hippocampus while, at the same time, there is a strengthening of synaptic connectivity through dendritic growth and spinogenesis in BLA.

These changes are called plastic remodeling and can last for some time. “... exposure to 10 days of chronic immobilization stress elicits dendritic hyertrophy [enhanced growth] in BLA principal neurons that lasts till at least 21 days after the termination of stress.”1 Meanwhile, the CA3 atrophy in the hippocampus is reported to be able to reverse these changes within the same period of post-stress recovery.1 In fact, the researchers explain that even a single 2 hour episode of immobilization that causes no dendritic atrophy in the BLA one day later can still result in a significant increase in spine density ten days later.

The authors also say, “in [mice genetically engineered to overexpress BDNF], overexpression of BDNF also causes spinogenesis in the BLA. Moreover, BLA spinogenesis is also triggered by chronic stress in control mice [that express BDNF at normal levels] but is occluded by BDNF overexpression, thereby suggesting a role for BDNF signaling in stress-induced plasticity in the amygdala.”1 As the authors point out, these differential changes in the two brain areas pose a “significant challenge for pharmacological interventions aimed at countering the effects of stress on amygdala and hippocampus.” They suggest that further elucidation of the mechanisms involved would be helpful in designing better treatments for stress-related psychiatric conditions such as post-traumatic stress disorder characterized by impaired cognition and high levels of fear and anxiety.

Reference

  1. Lakshminarasimhan and Chattarji. Stress leads to contrasting effects on the levels of brain derived neurotrophic factor in the hippocampus and amygdala. PLoS ONE 7(1):e30481 (Jan. 2012).

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