I plan to go on one of my strange tangents again! Please forgive me! I read this cool article called “CD4-Positive T Lymphocytes Provide a Neuroimmunological Link in the Control of Adult Hippocampal Neurogenesis.” Before you walk away screaming “MURDER,” give me a chance to explain. The general idea behind this article was that the immune system (my new favorite thing to talk about—honestly) plays a specific role in generating a microenvironment for baseline neurogenesis. To test this hypothesis, they used T/B Cell KO or mutated mice. They also played with cluster of differentiation (CD4) glycoproteins. This protein is expressed on the surface of T-cells–It’s the reason why HIV can infect T cells. Anyhow, the results suggest that depleting CD4 decreases Brdu+/DCX+ positive cells AND decreases BDNF production in the brain.
What does that sound like? Well, it sounds a lot like our discussions on depression. My question is should we be examining the shift of these immune system populations in depression? I once read a paper that looked at spleen/bone marrow cell populations from socially defeated rats. Most of the results were based on in vitro studies. So, why can’t we talk about immune system abnormalities that shift baseline neurogenesis? Maybe this shift predisposes people to depression.
I also have a big finale! Maybe it is not really a finale… So, the researchers in the immune system paper did a morris water maze test. By the way, Immunologists should get extra brownie points for doing behavioral studies! Okay, back to the subject!! In the water maze test, they found that CD4 depleted mice have a problem with the reversal learning phase. Let me back up. In this particular study, the test was divided into the acquisition phase (3 days), reversal learning phase (2 days), and the normal probe test. There was no significant difference between the learning curves or the latency to the center for the controls and CD4 depleted mice. When the platform was placed in the opposite quadrant (reversal learning phase), the latency times were significantly higher for the CD4 depleted mice compared to the controls. The researchers suggested that this reversal learning phase tests the ability to reconsolidate/relearn new situations. They eventually explain that neurogenesis is not extremely important in learning and memory, but “to avoid catastrophic interferences in relearning situations.” I think that sentence could drive a lot behavioral neuroscientists crazy, but that is not the point. What if a similar “conclusion” could be made about depression? What if these new neurons protect people from these “catastrophic episodes” that interfere with mood? The inability to create these new neurons might mean that the protection gets disrupted and people experience depression. It could also mean that all of this is under immune system function. Have we heard this before?
Think about it!