Learning Glia

There’s been a lot of discussion lately about Glia, Micro Glia, Glial Cells and Glia Cell Activation. It’s been noted that these cells play a role in RSD/CRPS.

The Living with HOPE Radio Show http://www.blogtalkradio.com/thebodymindandspiritnetwork with Host Trudy Thomas ran a weekly live feature on the topic titled “Glia, what is it?” with Guest Chris Greulich Writer and Editor of the Patient Awareness Blog http://www.patientawareness.org hosted by the Power of Pain Foundation.

The episodes are now in the shows archives for listening to either directly from the site for by downloading.

I myself find this fascinating and continue to learn all that I can. I encourage each of you to research what you can too. Some key words are listed above, you can also add RSD/CRPS to it. Other articles are located in my pages section and there will be more to come. We all need to take an active role in our own illness, read, research, talk with others who understand, listen and learn.

Remove all to as many possible stresses and triggers from your lives as these only cause the pain to escalate with Flare-Ups. Practice calm and appreciation.

From what we’ve learned so far the closest thing to deactivating the glia cell activation is Ketamine. Low dose Naltraxone is working to minimize the pain of some of those who’ve had the opportunity to try it, but not to the point of remission that Ketamine offers many.

I myself am no longer taking Morphine, or any of the Vicodin family, but instead Suboxone. I take it as my main pain reducer not to fight addiction.

I could return to one of the others, but I choose not to. As long as the Suboxone continues to work well enough, I’ll remain on it. I got to the point that my other pain relievers failed to ease me or take the edge off.

Many suffer from Opioid Induced Hyperalgesia and don’t even realize it. Yet are fearful to wean off their medications to find out. Trust me, I would be scared too, but sometimes we have to take that hard step forward even if it’s no longer literal to find out what’s best for us.

Time to learn much more about Glia and what else shuts down it’s activation.

I pray that if a cure doesn’t make it to us in my lifetime it will for certain in my children’s for who knows how many more million will be affected by then.

Nervous System with Glia

 

Nervous tissue consists of neurons, which are the cells that conduct signals, and supporting neuroglial cells such as microglial cells, astrocytes and oligodendrocytes.

Nerve – Bundle of nerve fibers outside the central nervous system.

Neuron – Nerve cell that characteristically has three parts: dendrites, cell body, and axon.

Neuroglial Cell – One of several types of cells found in nervous tissue that supports, protects, and nourishes neurons.

Microglia- A Promising Target for Treating Neuropathic Pain

Modulation of microglia can attenuate neuropathic pain symptoms and enhance morphine effectiveness.

Abstract

Microglia play a crucial role in the maintenance of neuronal homeostasis in the central nervous system, and microglia production of immune factors is believed to play an important role in nociceptive transmission. There is increasing evidence that uncontrolled activation of microglial cells under neuropathic pain conditions induces the release of proinflammatory cytokines (interleukin – IL-1beta, IL-6, tumor necrosis factor – TNF-alpha), complement components (C1q, C3, C4, C5, C5a) and other substances that facilitate pain transmission. Additionally, microglia activation can lead to altered activity of opioid systems and neuropathic pain is characterized by resistance to morphine. Pharmacological attenuation of glial activation represents a novel approach for controlling neuropathic pain. It has been found that propentofylline, pentoxifylline, fluorocitrate and minocycline decrease microglial activation and inhibit proinflammatory cytokines, thereby suppressing the development of neuropathic pain. The results of many studies support the idea that modulation of glial and neuroimmune activation may be a potential therapeutic mechanism for enhancement of morphine analgesia. Researchers and pharmacological companies have embarked on a new approach to the control of microglial activity, which is to search for substances that activate anti-inflammatory cytokines like IL-10. IL-10 is very interesting since it reduces allodynia and hyperalgesia by suppressing the production and activity of TNF-alpha, IL-1beta and IL-6. Some glial inhibitors, which are safe and clinically well tolerated, are potential useful agents for treatment of neuropathic pain and for the prevention of tolerance to morphine analgesia. Targeting glial activation is a clinically promising method for treatment of neuropathic pain.

Microglia: a promising target for treating neuropathic and postoperative pain, and morphine tolerance.

Source

Department of Anesthesiology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA.

Abstract

Management of chronic pain, such as nerve-injury-induced neuropathic pain associated with diabetic neuropathy, viral infection, and cancer, is a real clinical challenge. Major surgeries, such as breast and thoracic surgery, leg amputation, and coronary artery bypass surgery, also lead to chronic pain in 10-50% of individuals after acute postoperative pain, partly due to surgery-induced nerve injury. Current treatments mainly focus on blocking neurotransmission in the pain pathway and have only resulted in limited success. Ironically, chronic opioid exposure might lead to paradoxical pain. Development of effective therapeutic strategies requires a better understanding of cellular mechanisms underlying the pathogenesis of neuropathic pain. Progress in pain research points to an important role of microglial cells in the development of chronic pain. Spinal cord microglia are strongly activated after nerve injury, surgical incision, and chronic opioid exposure. Increasing evidence suggests that, under all these conditions, the activated microglia not only exhibit increased expression of microglial markers CD 11 b and Iba 1, but also display elevated phosphorylation of p38 mitogen-activated protein kinase. Inhibition of spinal cord p38 has been shown to attenuate neuropathic and postoperative pain, as well as morphine-induced antinociceptive tolerance. Activation of p38 in spinal microglia results in increased synthesis and release of the neurotrophin brain-derived neurotrophic factor and the proinflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α. These microglia-released mediators can powerfully modulate spinal cord synaptic transmission, leading to increased excitability of dorsal horn neurons, that is, central sensitization, partly via suppressing inhibitory synaptic transmission. Here, we review studies that support the pronociceptive role of microglia in conditions of neuropathic and postoperative pain and opioid tolerance. We conclude that targeting microglial signaling might lead to more effective treatments for devastating chronic pain after diabetic neuropathy, viral infection, cancer, and major surgeries, partly via improving the analgesic efficacy of opioids.

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