Destruction of glial cells results in depression
The human brain is the most complex organ in the body. It is composed of cells called neurons, which transmit signals to one another. There are billions of neurons in one human’s brain and many different types that play different roles in the complex signaling pathways. The brain is responsible for mood, emotions, cognition and physiological mechanisms such as breathing, hormonal release, temperature control, heart rate and sexual drive. When signaling in the brain goes awry due to either neuronal mishaps or a defect in the neurotransmitter release, psychological disorders such as depression, bipolar disease and even schizophrenia occur.
What are glial cells?
Glial cells are non-neuronal cells that play a major role in the support and protection of neurons. The word “glial” translates to glue in the Greek language. They are very different from neurons because they do not participate in communication or cell signaling but rather they help build and support neurons that are responsible for sending signals to each other. Glial cells outnumber neuronal cells in the nervous system by a 3-to-1 ratio. There are three different types of glial cells that help serve different functions: astrocytes, microglial cells and oligodendrocytes. Their respective roles are to maintain a proper signaling environment, function as stem cells and to produce myelin, which is the insulation that helps conduct signals between neurons.
The link between the destruction of glial cells and depression
A recent study was published in the journal Neuron that illustrated the importance of glial cells and their link to depression in human. The destruction of NG-2 glial cells in the prefrontal cortex results in depression in humans. The specific mechanism is not well understood, however it is known that the destruction of the NG-2 glial cells results in a depletion of the excitatory neurotransmitter glutamate. This is one of the most important neurotransmitters in the brain, and over half of all the neuronal synapses release this chemical. The dysregulation of glutamate is responsible for a few serious neurological diseases including Alzheimer diseases, stroke, epilepsy and amyotrophic lateral sclerosis (ALS) or more commonly known as Lou Gehrig’s disease. With playing such a powerful role in the nervous system, it is not surprising that glial cells can play a major role in depression.
“We found that when NG2 glia, and consequently the production of FGF2 (growth factors), are decreased, depressive-like behaviors take hold,” said Dr. Aguirre. “Conversely, when the abundance of NG2 glia is returned to normal levels, the depressive-like behaviors cease.” The researchers used genetic manipulations to ablate NG2 glia in the prefrontal cortex of adult mice. This caused deficits in neurotransmission and other brain processes that induced depressive-like behavior. The team similarly demonstrated that blocking NG2 glial secretion of FGF2 induces the same depressive behaviors.”
New research may bring new treatments
Major depressive disorder affects approximately 15 million American adults in a given year. The mainstay of therapy is a class of antidepressants known as selective serotonin re-uptake inhibitors (SSRIs), which act to increase serotonin in the brain. It is widely known that over time a chronic increase in serotonin suppresses the dopaminergic system in the brain. This results in disarray, so antidepressants are meant to be used for a short-term treatment to get over the hump. This riveting new research on the role glial cells play on depression can potentially lead researchers to develop another type of therapy that targets depression.
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About the Author
Kristen Fuller, M.D., is a senior staff writer at Sovereign Health Group and enjoys writing about evidence-based topics in the cutting-edge world of medicine. She is a physician and author who also teaches, practices medicine in the urgent care setting and contributes to medicine board education. She is also an outdoor and dog enthusiast. For more information and other inquiries about this article, contact the author at firstname.lastname@example.org.