Depressed individuals need support. Yes, of course they need social support, but I’m talking a little more specific here. Depressed people need NEURAL support–yes, their neurons need support. Actual, structural support. Perhaps combined, these hold the answer to a cure.
After our discussion in class regarding the loss of volume in depressed (and other psychological disorders) patients, it really got me thinking. The article we read mentioned how small of a percentage of total volume new neurons in the dentate gyrus actually contribute over the lifetime. This small percentage cannot account for the significant loss of volume on its own–there must be something else co-occuring, or perhaps even predating, this loss of neurogenesis in order to facilitate the depression. I looked around and found an interesting paper that addresses the possibility that glial cells are actually a significant contributor to depression (interestingly enough, this paper was co-authored by Duman, one of the authors on our assigned reading for today!!).
Banasr, M., & Duman, R.S. (2008). Glial loss in the prefrontal cortex is sufficient to induce depressive-like behaviors. Biological Psychiatry, 64, 863-870.
ABSTRACT: BACKGROUND: Postmortem studies have repeatedly found decreased density and number of glia in cortical regions, including the prefrontal and cingulate areas, from depressed patients. However, it is unclear whether this glial loss plays a direct role in the expression of depressive symptoms. METHODS: To address this question, we characterized the effects of pharmacologic glial ablation in the prefrontal cortex (PFC) of adult rats on behavioral tests known to be affected by stress or antidepressant treatments: sucrose preference test (SPT), novelty suppressed feeding test (NSFT), forced swim test (FST), and two-way active avoidance test (AAT). We established the dose and time course for the actions of an astrocyte specific toxin, L-alpha-aminoadipic acid (L-AAA), and compared the behavioral effects of this gliotoxin with the effects of an excitotoxic (ibotenate) lesion and to the effects of chronic stress. RESULTS: The results demonstrate that L-AAA infusions induced anhedonia in SPT, anxiety in NSFT, and helplessness in FST and AAT. These effects of L-AAA were similar to chronic unpredictable stress (CUS)-induced depressive-like behaviors in these tests. However, ibotenate-induced neurotoxic lesion of the PFC had no effect in these behavioral tests. CONCLUSIONS: The results demonstrate that glial ablation in the PFC is sufficient to induce depressive-like behaviors similar to chronic stress and support the hypothesis that loss of glia contributes to the core symptoms of depression.
WOW. So how does this fit in with what we discussed today in class? This seems to completely support our hypothesis that you need these support systems for the new neurons in order to effectively (possibly) treat depression. What if depression actually begins as a problem with glial cells?? If this is truely a possibility, I think we should be putting a lot of resources toward this question in order to better support individuals with depression and advance treatment options.