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.
On Psychology and Neuroscience 
Nice idea Jenn! It would sure be interesting if it was really all up to the glial cells instead of the neurons like we have thought all along! I think this merits some further research and if anything glial cells do play a part in depression.
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This is a really interesting idea. It just goes to show once again how little we actually know about what is causing depression. It also seems very promising that there seem to be so many areas involved. Maybe this will continue to give us more treatment options for major depression in the future.
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Great entry Jenn. Scientists should pay more attention to glial cells. They account for a lot in neurogenesis and the increase in hippocampal volume. What a wonderful idea. I would fund this project.
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Wow, Sharonda. What other projects will you be funding?!
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oohhh Lia 🙂 Anything that sounds/looks promising. Send me an abstract if you want $$$. I’ll pull some strings.
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This was interesting because the article we just read for class dealt with the fact that there is much reproduction of glial cells all parts of the brain, and possibly only neurogenesis of neurons in certain, older parts of the brain. The physical treatment for depression would seem to be much closer if it is truely the glial cells that are the problem causing depression. The glial cells, it would seem, would be much easier to induce into mitosis.
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Jenn, I really like the point you have made here. As Hannah mentioned, it does just really show us how much we DON’T know about depression and it’s causes, and related back to the dopaminergic reward circuit in depression paper, in that there are so many area’s that are related to depression. Even though the serotonin NT system seems to play a big role in depression, this gives rise to the idea that it’s not just irregulation with that system, but others as well!
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Jenn, your entry is really interesting. I think you make an incredibly valid point that current science should definitely further investigate. It’s funny how we always look at depression as a disease that can be treated, but never fully cured because the cause or causes of it are still unknown. With your observation that maybe depression’s roots lie in glial cells, not only neurons, modern science can begin to see the cause of depression and act accordingly to potentially cure it. You have a great idea here, I hope further research is conducted!
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Really interesting study Jenn! After reading the abstract I read more about some of the secondary functions of astrocytes, which the researchers ablated in this study. I found it interesting that beyond the normal functions of support, clean-up, and nutrient supply, they also play a key role in maintaining the chemical balance of the fluid surrounding neurons. A degradation of these glia could no doubt disrupt the regular transmission of NT across the synapse. The mention of the pre-frontal cortex, in addition, reminded me of the Phineas Gage case in which, after the destruction of his PFC, he was known to be an irritable man: unlike the person he once was.
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This is a really interesting and new idea. In past experience, it seems to me that most people relate psychological disorders with a loss of neurons rather than glial cells. If this is true, then maybe depression can be prevented before a person even begins to show the symptoms. The question is: Does depression, because it causes a level of despair, cause a decrease in the rate of production of glial cells, or does a degeneration of glial cells cause depression?
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I was surprised to find in reading this post that glial cells could be linked to depression. I’d always heard that this disorder was caused when serotonin was not binding enough to its receptors. I never really thought about there being other causes so this was rather eye-opening for me. I think it makes sense that glial deficits would contribute to depression since people afflicted with depression tend to experience a “slower” rate of thinking. I’d be interested in finding out more about what causes the reduced production of glial cells.
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This is cool! And definitely still fits the neurogenesis idea, because we know the debate over whether the new neurons are actually neurons… or glial cells?! (poor gould).
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